Warning: Illegal string offset 'lang' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 350

Warning: Illegal string offset 'keywords' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 354

Warning: Illegal string offset 'description' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 356

Warning: Illegal string offset 'lang' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 353

Warning: Illegal string offset 'keywords' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 354

Warning: Illegal string offset 'description' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 356

Warning: Illegal string offset 'lang' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 353

Warning: Illegal string offset 'keywords' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 354

Warning: Illegal string offset 'description' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 356

Warning: Illegal string offset 'lang' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 353

Warning: Illegal string offset 'keywords' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 354

Warning: Illegal string offset 'description' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 356

Warning: Illegal string offset 'lang' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 353

Warning: Illegal string offset 'keywords' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 354

Warning: Illegal string offset 'description' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 356

Warning: Illegal string offset 'lang' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 353

Warning: Illegal string offset 'keywords' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 354

Warning: Illegal string offset 'description' in /home1/roskampi/public_html/articles/wp-content/plugins/keyword-statistics/keyword-statistics.php on line 356

Roskamp Institute Articles Better Science. Real Discovery.

August 2, 2012

Event: Journal Club ” A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline.”

Filed under: Uncategorized — Tags: , , — Gogce Crynen @ 1:04 pm

We will be presenting the paper on Friday (7/20/2012) at 4:00 PM in Roskamp Institute. Title: A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline.

Jonsson T, Atwal JK, Steinberg S, Snaedal J, Jonsson PV, Bjornsson S, Stefansson H, Sulem P, Gudbjartsson D, Maloney J, Hoyte K, Gustafson A, Liu Y, Lu Y, Bhangale T, Graham RR, Huttenlocher J, Bjornsdottir G, Andreassen OA, Jönsson EG, Palotie A, Behrens TW, Magnusson OT, Kong A, Thorsteinsdottir U, Watts RJ, Stefansson K. A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline. Nature. 2012 Jul 11. doi: 10.1038/nature11283. [Epub ahead of print]

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.
The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949.

June 4, 2012

Event: Journal Club ” Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells “.

Filed under: Uncategorized — Tags: , , , — Gogce Crynen @ 12:53 pm

We will be presenting the paper on Friday (6/8/2012) at 4:00 PM in Roskamp Institute. Title:  ” Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells “.

Israel MA, Yuan SH, Bardy C, Reyna SM, Mu Y, Herrera C, Hefferan MP, Van Gorp S, Nazor KL, Boscolo FS, Carson CT, Laurent LC, Marsala M, Gage FH, Remes AM, Koo EH, Goldstein LS. Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells. Nature. 2012 Feb 9;482(7384):216-20.

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949.

May 14, 2012

Event: Journal Club “Proline Isomer-Specific Antibodies Reveal the Early Pathogenic Tau Conformation in Alzheimer’s Disease “.

Filed under: Uncategorized — Tags: , , — Gogce Crynen @ 3:04 pm

Alex Bishop will be presenting the paper on Friday (5/18/2012) at 4:00 PM in Roskamp Institute. Title:  “Proline Isomer-Specific Antibodies Reveal the Early Pathogenic Tau Conformation in Alzheimer’s Disease “.
Kazuhiro Nakamura, Alex Greenwood, Lester Binder, Eileen H. Bigio, Sarah Denial, Linda Nicholson, Xiao Zhen Zhou, and Kun Ping Lu, Proline Isomer-Specific Antibodies Reveal the Early Pathogenic Tau Conformation in Alzheimer’s Disease, Cell, 149(1), March 2012, Pages 232-244
Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949.

March 9, 2012

NILVAD

Filed under: Uncategorized — Tags: , , , — Gogce Crynen @ 12:15 pm

To learn about NILVAD project partners and for more information on NILVAD please follow the link:

http://www.alzheimer-europe.org/News/Alzheimer-Europe/Wednesday-15-February-2012-NILVAD-project-team-holds-first-meeting-in-Dublin

January 30, 2012

Event: Journal Club ” Alzheimer’s disease and non-demented high pathology control nonagenarians: comparing and contrasting the biochemistry of cognitively successful aging. ”

Filed under: Uncategorized — Tags: , — Gogce Crynen @ 2:03 pm

Benoit Mouzon will be presenting the paper on Friday (2/3/2012) at 4:00 PM in Roskamp Institute.
Title: “ Alzheimer’s disease and non-demented high pathology control nonagenarians: comparing and contrasting the biochemistry of cognitively successful aging.”

Maarouf CL, Daugs ID, Kokjohn TA, Walker DG, Hunter JM, Kruchowsky JC, Woltjer R, Kaye J, Castaño EM, Sabbagh MN, Beach TG, Roher AE. Alzheimer’s disease and non-demented high pathology control nonagenarians: comparing and contrasting the biochemistry of cognitively successful aging. PLoS One. 2011;6(11):e27291. Epub 2011 Nov 7.

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.
The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

January 23, 2012

Event: Journal Club ” Directed Conversion of Alzheimer’s Disease Patient Skin Fibroblasts into Functional Neurons “

Filed under: Uncategorized — Tags: , , — Gogce Crynen @ 1:11 pm

Alex Bishop will be presenting the paper on Friday (1/13/2012) at 4:00 PM in Roskamp Institute.
Title: ” Directed Conversion of Alzheimer’s Disease Patient Skin Fibroblasts into Functional Neurons ”

Liang Qiang, Ryousuke Fujita, Toru Yamashita, Sergio Angulo, Herve Rhinn, David Rhee, Claudia Doege, Lily Chau, Laetitia Aubry, William B. Vanti et al. 2011. Directed Conversion of Alzheimer’s Disease Patient Skin Fibroblasts into Functional Neurons. Cell. 146(3) pp. 359 – 371.

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

January 5, 2012

Event: Journal Club ” Oral bioavailability of the ether lipid plasmalogen precursor, PPI-1011, in the rabbit: a new therapeutic strategy for Alzheimer’s disease ”

Filed under: Uncategorized — Tags: , , — Gogce Crynen @ 12:38 pm

Laila Abdullah will be presenting the paper on Friday (1/6/2012) at 4:30 PM in Roskamp Institute.

Title: “Oral bioavailability of the ether lipid plasmalogen precursor, PPI-1011, in the rabbit: a new therapeutic strategy for Alzheimer’s disease ”

Wood PL, Smith T, Lane N, Khan MA, Ehrmantraut G, Goodenowe DB. Oral bioavailability of the ether lipid plasmalogen precursor, PPI-1011, in the rabbit: a new therapeutic strategy for Alzheimer’s disease. Lipids Health Dis. 2011 Dec 5;10(1):227. [Epub ahead of print]

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

August 15, 2011

Event: Journal Club ” Docosahexaenoic acid-derived neuroprotectin D1 induces neuronal survival via secretase- and PPARγ-mediated mechanisms in Alzheimer’s disease models.”

Filed under: Uncategorized — Tags: , , , , — Gogce Crynen @ 10:44 am

Laila Abdullah will be presenting the paper on Friday (8/19/2011) at 4:00 PM in Roskamp Institute.

Title: ” Docosahexaenoic acid-derived neuroprotectin D1 induces neuronal survival via secretase- and PPARγ-mediated mechanisms in Alzheimer’s disease models.”

Zhao Y, Calon F, Julien C, Winkler JW, Petasis NA, Lukiw WJ, Bazan NG. Docosahexaenoic acid-derived neuroprotectin D1 induces neuronal survival via secretase- and PPARγ-mediated mechanisms in Alzheimer’s disease models. PLoS One. 2011 Jan 5;6(1):e15816.

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

July 26, 2011

Event: Journal Club ” Nicotinic acetylcholine receptor signalling: roles in Alzheimer’s disease and amyloid neuroprotection.” and ” Alpha7 neuronal nicotinic receptors: the missing link to understanding Alzheimer’s etiopathology?”

John Phillips will be presenting the paper on Friday (7/29/2011) at 4:00 PM in Roskamp Institute.

Title: ” Nicotinic acetylcholine receptor signalling: roles in Alzheimer’s disease and amyloid

neuroprotection.” and ” Alpha7 neuronal nicotinic receptors: the missing link to understanding Alzheimer’s etiopathology?”

Buckingham SD, Jones AK, Brown LA, Sattelle DB. Nicotinic acetylcholine

receptor signalling: roles in Alzheimer’s disease and amyloid

neuroprotection. Pharmacol Rev. 2009 Mar;61(1):39-61. Epub 2009 Mar 16.

Bencherif M, Lippiello PM. Alpha7 neuronal nicotinic receptors: the missing

link to understanding Alzheimer’s etiopathology? Med Hypotheses. 2010

Feb;74(2):281-5. Epub 2009 Oct 1.

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

May 25, 2011

ALZHEIMER’S DISEASE DRUG DEVELOPED AT ROSKAMP INSTITUTE APPROVED FOR KEY CLINICAL TRIAL FUNDING IN EUROPE

Filed under: Uncategorized — Tags: , , , , — Gogce Crynen @ 10:08 am

ALZHEIMER’S DISEASE DRUG DEVELOPED AT ROSKAMP INSTITUTE

APPROVED FOR KEY CLINICAL TRIAL FUNDING IN EUROPE

SARASOTA, FL – An international research consortium led by Trinity College Dublin (Ireland) today announced the selection for funding of a large-scale European clinical trial of Nilvadipine, an Alzheimer’s disease drug developed at the Roskamp Institute in Sarasota. More than 500 Alzheimer’s patients will participate in the multicenter Phase III clinical trial designed to study the effectiveness of Nilvadipine.

“We need many more medicines to move forward into advanced clinical trials in the fight against Alzheimer’s Disease and we are pleased the Roskamp Institute has played such a major role in the development of this drug,” said Michael Mullan, M.D., Ph.D., Roskamp Institute director who, with associate director Fiona Crawford, Ph.D. and lead scientist Daniel Paris, Ph.D., led the research team that developed the drug.  Phase III studies are usually the last step in the regulatory process before a drug can move into clinical practice.

“Only a handful of Alzheimer’s drugs have ever reached this stage, and most were developed by major pharmaceutical companies.  It’s a tremendous achievement for a research institute like ours to be part of the process,” said Crawford.

Brian Lawlor, M.D., Connolly Norman Professor of Old Age Psychiatry at Trinity College Dublin, Ireland, will be principal investigator and coordinator of the US$ 8.4 million Nilvadipine study, which is being funded by the European Commission Seventh Framework Programme.  More than 20 European clinical sites will participate in the placebo-controlled study.  Anticipated to begin in early 2012, patients with mild to moderate Alzheimer’s disease will be recruited to participate.

“Considering the devastating impact that Alzheimer’s disease has on people, there is relatively little research funding being made available to tackle this major killer,” said Lawlor.

The clinical trials will take place in Europe, where Nilvadipine is already approved for use in mild cases of hypertension (high blood pressure). “The process can move more quickly in Europe, and the study findings may help accelerate the process with the U.S. Food and Drug Administration (FDA),” Mullan said.

Mullan and Crawford have been studying Alzheimer’s disease for more than 20 years, moving from the UK to Florida in 1991 and to Sarasota in 2003 to establish the Roskamp Institute.  “Some of our recent studies have involved Sarasota area residents, who have contributed to our understanding of Alzheimer’s disease and helped move the development process forward,” said Crawford.

In the Sarasota laboratories, the research team discovered that Nilvadipine, a drug approved in Europe for treatment of hypertension, can stop the accumulation of the amyloid proteins in the brain – a development that has been implicated in Alzheimer’s disease. A combined Phase I/II clinical trial was completed in Europe by the Institute last year and focused on Nilvadipine’s safety. “The initial results indicated that patients with Alzheimer’s disease were able to tolerate the drug well,”   said Mullan.

Now, the Roskamp Institute will provide research support for the Phase III clinical trial, such as assessing genetic and other markers for Alzheimer’s disease in study participants.

The Institute’s commercial spinoff, Archer Pharmaceuticals, owns the intellectual property rights to Nilvadipine, and Mullan serves as Archer’s chief executive officer.  “There are always risks involved with drug development and discovery,” said Mullan. “But we must continue to invest in new approaches in the worldwide battle against Alzheimer’s disease.”

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. The Institute is located in Sarasota, Florida, and operates a memory clinic onsite.

For more information:  www.rfdn.org

Contact:  Steve Klindt

Tel: 941-752-2949

Email: sklindt@roskampinstitute.org

April 11, 2011

Event: Journal Club ” Psychosis in Alzheimer’s Disease in the National Alzheimer’s Disease Coordinating Center Uniform Data Set: Clinical Correlates and Association with Apolipoprotein E ” and ” Apolipoprotein E regulates the integrity of tight junctions in an isoform-dependent manner in an in vitro blood-brain-barrier model “

Filed under: Uncategorized — Tags: , , , , , , , — Gogce Crynen @ 2:13 pm

Ekta Shah will be presenting the paper on Friday (4/15/2011) at 4:00 PM in Roskamp Institute.

Title: ” Psychosis in Alzheimer’s Disease in the National Alzheimer’s Disease Coordinating Center Uniform Data Set: Clinical Correlates and Association with Apolipoprotein E ” and ” Apolipoprotein E regulates the integrity of tight junctions in an isoform-dependent manner in an in vitro blood-brain-barrier model ”

International Journal of Alzheimer’s Disease, Volume 2011 (2011), Article ID 926597, 8 pages

doi:10.4061/2011/926597 and  JBC, 2011, doi: 10.1074/jbc.M111.225532 , respectively.

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

March 14, 2011

Event: Journal Club “Reversing EphB2 depletion rescues cognitive functions in Alzheimer model”

Filed under: Uncategorized — Tags: , , , , — Gogce Crynen @ 2:24 pm

John Phillips will be presenting the paper on Friday (3/18/2011) at 4:00 PM in Roskamp Institute.

Title: Reversing EphB2 depletion rescues cognitive functions in Alzheimer model

6 JANUARY 201 1 | VOL 469 | NATURE | 47

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

March 7, 2011

Event: Journal Club “High ability of apolipoprotein E4 to stabilize amyloid-peptide oligomers, the pathological entities responsible for Alzheimer’s disease”

Filed under: Uncategorized — Tags: , , , , , — Gogce Crynen @ 11:27 am

Laila Abdullah will be presenting the paper on Friday (3/4/2011) at 4:00 PM in Roskamp Institute.


Title: High ability of apolipoprotein E4 to stabilize amyloid-peptide oligomers, the pathological entities responsible for Alzheimer’s disease

FASEB J. 2011 Jan 25. [Epub ahead of print]

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

February 1, 2011

Event: Journal Club “Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer’s disease. ”

Filed under: Uncategorized — Tags: , — Gogce Crynen @ 10:09 am

Ekta Shah will be presenting the paper on Friday (2/4/2011) at 4:00 PM in Roskamp Institute.

Title: Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer’s disease.

J Biol Chem. 2010 Nov 30. [Epub ahead of print]

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

January 17, 2011

Event: Journal Club “The characterization of microtubule-stabilizing drugs as possible therapeutic agents for Alzheimer’s disease and related tauopathies”

Filed under: Uncategorized — Tags: , — Gogce Crynen @ 10:15 am

Chris Mayer will be presenting the paper on Friday (1/21/2011) at 4:00 PM in Roskamp Institute.

Title: The characterization of microtubule-stabilizing drugs as possible therapeutic agents for Alzheimer’s disease and related tauopathies

Pharmacol Res. 2010 Dec 14. [Epub ahead of print]

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

December 22, 2010

Selective antihypertensive dihydropyridines lower Aβ accumulation by targeting both the production and the clearance of Aβ across the blood-brain barrier

Abstract

Several large population based or clinical trial studies have suggested that certain dihydropyridine (DHP) L-type calcium channel blockers (CCBs) used for the treatment of hypertension may confer protection against the development of Alzheimer’s disease (AD). However, other studies with drugs of the same class have shown no beneficial clinical effects. In order to determine whether certain DHPs are able to impact underlying disease processes in AD (specifically the accumulation of the Alzheimer’s Aβ peptide), we investigated the effect of several antihypertensive DHPs and non-DHP CCBs on Aβ production. Among the antihypertensive DHPs tested, a few, including nilvadipine, nitrendipine and amlodipine inhibited Aβ production in vitro whereas others had no effect or raised Aβ levels. In vivo, nilvadipine and nitrendipine acutely reduced brain Aβ levels in a transgenic mouse model of AD (Tg PS1/APPsw) and improved Aβ clearance across the blood-brain barrier (BBB) whereas amlodipine and nifedipine were ineffective showing that the Aβ lowering activity of the DHPs is independent of their antihypertensive activity. Chronic oral treatment with nilvadipine decreased Aβ burden in the brains of Tg APPsw (Tg2576) and Tg PS1/APPsw mice and also improved learning abilities and spatial memory. Our data suggest that the clinical benefit conferred by certain antihypertensive DHPs against AD is unrelated to their antihypertensive activity but rely on their ability to lower brain Aβ accumulation by affecting both Aβ production and Aβ clearance across the BBB.

Paris DBachmeier CPatel NQuadros AVolmar CHLaporte VGaney JBeaulieu-Abdelahad DAit-Ghezala GCrawford FMullan MJ.

Mol Med. 2010 Dec 17. [Epub ahead of print]

Characterization and Use of Human Brain Microvascular Endothelial Cells to Examine β-amyloid Exchange in the Blood-Brain Barrier

Dr. Bachmeier and Dr. Paris recently published an article in Cytotechnology entitled “Characterization and Use of Human Brain Microvascular Endothelial Cells to Examine β-amyloid Exchange in the Blood-Brain Barrier”. They are currently using this model of the BBB to elucidate the mechanisms responsible for the removal of β-amyloid from the brain. In addition, this model is being used as a screen to identify molecules that facilitate β-amyloid clearance across the BBB with the goal of discovering a new class of therapies for the treatment of Alzheimer’s disease.

Abstract Alzheimer’s disease (AD) is characterized by excessive cerebrovascular deposition of the β-amyloid peptide (Aβ). The investigation of Aβ transport across the blood-brain barrier (BBB) has been hindered by inherent limitations in the cellular systems currently used to model the BBB, such as insufficient barrier properties and poor reproducibility. In addition, many of the existing models are not of human or brain origin and are often arduous to establish and maintain. Thus, we characterized an in vitro model of the BBB employing human brain microvascular endothelial cells (HBMEC) and evaluated its utility to investigate Aβ exchange at the blood-brain interface. Our HBMEC model offers an ease of culture compared with primary isolated or coculture BBB models and is more representative of the human brain endothelium than many of the cell lines currently used to study the BBB. In our studies, the HBMEC model exhibited barrier properties comparable to existing BBB models as evidenced by the restricted permeability of a known paracellular marker. In addition, using a simple and rapid fluormetric assay, we showed that antagonism of key Aβ transport proteins significantly altered the bi-directional transcytosis of fluorescein-Aβ (1-42) across the HBMEC model. Moreover, the magnitude of these effects was consistent with reports in the literature using the same ligands in existing in vitro models of the BBB. These studies establish the HBMEC as a representative in vitro model of the BBB and offer a rapid fluorometric method of assessing Aβ exchange between the periphery and the brain.

November 16, 2010

Event: Journal Club, Neuroscience San Diego 2010 meeting highlights

Filed under: Uncategorized — Tags: , , , , — Gogce Crynen @ 10:51 am
Please join us at 4:00 pm this Friday at the Roskamp Institute for Journal Club. We will have a special presentation by Laila Abdullah, Scott Ferguson, and Benoit Mouzon of the highlights of the 2010 Society for Neuroscience conference.

Journal Club is held every Friday. For change in schedule please check our Twitter account or Facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

November 3, 2010

Event: Journal Club “Gamma-secretase activating protein is a therapeutic target for Alzheimer’s disease”

Filed under: Uncategorized — Tags: , , , — Gogce Crynen @ 5:24 pm

John Phillips will be presenting the paper on Friday (11/05/2010) at 4:30 PM in Roskamp Institute.

Title: Gamma-secretase activating protein is a therapeutic target for Alzheimer’s disease.

Vol 467| 2 September 2010| doi:10.1038/nature09325

Journal Club is held every Friday. For change in schedule please check our twitter account or facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

September 22, 2010

Event: Journal Club “Amyloid-beta-42 signals tau hyperphosphorylation and compromises neuronal viability by disrupting alkylacylglycerophosphocholine metabolism”

Filed under: Uncategorized — Tags: , , , , — Gogce Crynen @ 9:37 am
Laila Abdullah will be presenting the paper on Friday (9/24/2010) at Roskamp Institute.

Title:  Amyloid-beta-42 signals tau hyperphosphorylation and compromises neuronal viability by disrupting alkylacylglycerophosphocholine metabolism.

PNAS, December 8, 2009, vol. 106, no. 49, 20936–20941

Journal Club is held every Friday between 4 pm-5pm. For change in schedule please check our twitter account or facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

September 13, 2010

News:Scientific team at the Roskamp Institute found evidence to support that processes controlling the growth of cerebral blood vessels are altered in the brains of transgenic mouse models of Alzheimer’s disease

Sarasota, Florida). Scientists at the Roskamp Institute in Sarasota, in collaboration with researchers from the H. Lee Moffitt Cancer Center in Tampa, have found laboratory evidence that the processes controlling the growth of cerebral blood vessels are altered  in the brains of transgenic mouse models of Alzheimer’s disease (AD). Scientists say the discovery will provide a better understanding of the role of cerebrovascular lesions in AD brains and may explain why vascular insults synergistically precipitate the cognitive presentation of AD. In addition, their research may provide new therapeutical approaches which are desperately needed to tackle this devastating disorder. AD is the most common form of dementia among the aging population and is characterized by the intracerebral accumulation of a small protein called b-amyloid, as well as, neurofibrillary tangles that form in the neurons of the affected patients. In addition to neuronal damages, AD brains also present evidence of capillary degeneration and a reduction in brain capillary density which probably contribute to the decreased cerebral blood flow reported in all patients suffering from the disease. The growth of blood vessels (or angiogenesis) is controlled by the balance between several growth factors that can stimulate their growth and other molecules that inhibit their formation. The amount of growth factors that normally stimulate angiogenesis is elevated in AD brains, which could suggest that the growth of cerebrovessels would be stimulated in AD. The growth of tumors is dictated by their vascularization, this is particularly true for brain tumors which are highly vascularized. Therefore, in order to determine whether angiogenesis was possibly altered in AD brains, the researchers implanted brain tumors in transgenic mouse models of AD (that have been genetically engineered to reproduce some of the AD brain pathology) as well as normal mice and measured the growth of the tumors in the animals. “Interestingly, we observed that the growth and vascularization of brain tumors was reduced in transgenic mouse models of AD compared to normal mice, suggesting that the AD brain does not constitute a favorable environment to support the growth of new blood vessels.” said Dr. Daniel Paris of the Roskamp Institute, lead author of the study published in the Journal of Neuroscience (J. Neurosci. 2010;30(34):11251-8). “Our data suggest the growth of new brain capillaries that takes place following a stroke for example, and allows for a restoration of the cerebral blood flow in the damage area, will be inhibited in AD. This may explain why vascular insults such as stroke are known to accelerate the cognitive decline in AD patients. Overall, our work suggests that therapies stimulating brain vascularization may be beneficial in AD patients.”, Dr. Paris added. Epidemiological studies have highlighted that the incidence of cancer is reduced in AD patients whereas the prevalence of AD is reduced in patients with an history of cancer suggesting a biological link between cancer and AD. “As the growth of blood vessels is required for the development of tumors, our work suggesting some impairment in the growth of blood vessels in AD may provide a biological mechanism explaining this intriguing relationship between cancer and AD.”, Dr. Paris said. The Roskamp Institute is a not-for-profit research Institute located in Sarasota, Fla., that is dedicated to understanding the causes of, and finding cures for, neuropsychiatric and neurodegenerative disorders with an emphasis on Alzheimer’s disease. The Institute’s Memory Clinic also offers comprehensive cognitive and medical assessment toward differential diagnosis of Alzheimer’s disease and offers treatments and disease management options once the diagnostic evaluation is complete. For more information, please contact the Institute at (941) 752-2949, Roskamp’s Clinical Trials Division in Sarasota at (941) 256-8018 or visit www.RoskampInstitute.com.

September 2, 2010

Event: Journal Club “Allopregnanolone levels are reduced in temporal cortex in patients with Alzheimer’s disease compared to cognitively intact control subjects”


Alex Bishop will be presenting the paper on Friday (9/3/2010) at Roskamp Institute.

Title:  “Allopregnanolone levels are reduced in temporal cortex in patients with Alzheimer’s disease compared to cognitively intact control subjects”

Biochimica et Biophysica Acta 1801 (2010) 951–959

Journal Club is held every Friday between 4 pm-5pm. For change in schedule please check our twitter account or facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

August 6, 2010

Governor Charlie Crist visits Roskamp Institute

Filed under: news — Tags: , , , — Gogce Crynen @ 1:28 pm

Governor Charlie Crist visited our Institute on Thursday, and was briefed about the most recent scientific breakthroughs that have occurred at the Institute, followed by a full tour of the laboratories.  Impressed with what he saw, Gov. Crist referred to the Institute as “Florida’s best-kept scientific secret.”

Alzheimer’s disease is a growing epidemic in Florida, and the Governor and Senatorial candidate was receptive to concerns raised by Institute scientists regarding future funding opportunities for Alzheimer’s research. There is currently no State funding for Alzheimer’s research in Florida, despite this state being one of the hardest hit by this devastating disease.  When such funds once more become available it is hoped that they will be distributed using a peer-review process (as used for State funding of Cancer research) so that the tax payers receive most “bang for their buck” with the best research programs receiving the funding.

The visit underscores the growing prominence of the Roskamp Institute within the Sarasota/Manatee community and greater local recognition for the Institute’s nationally and internationally recognized contributions to research progress in Alzheimer’s Disease, Cancer and other disorders. Gov. Crist also discussed the Institute’s research programs that are of critical importance to the military and veterans populations – Traumatic Brain Injury, Post Traumatic Stress Disorder and Gulf War Illness.  He was also interested in the innovative Ph.D. program now flourishing at Roskamp, as well as the Institute’s for-profit spin off, Archer Pharmaceuticals.

Gov. Crist’s visit was the most recent in a series of high-profile visits to the Institute, which have included visits from Senator Bill Nelson and Congressman C. W. Bill Young.  James Humphrey, Roskamp COO was encouraged by the visit, as it was yet another means by which the the Institute can “reach out into the public domain” and raise awareness of the scope of research being conducted in the Sarasota/Manatee area

July 19, 2010

Event: Journal Club “Lysosomal Proteolysis and Autophagy Require Presenilin 1 and Are Disrupted by Alzheimer-Related PS1 Mutations”

Filed under: alzheimer — Tags: , , , , , — Gogce Crynen @ 4:17 pm


John Phillips will be presenting the paper on Friday (7/30/2010) at Roskamp Institute.

Title: Lysosomal Proteolysis and Autophagy Require Presenilin 1 and Are Disrupted by Alzheimer-Related PS1 Mutations

Journal: Cell

Volume 141, Issue 7, 1146-1158, 10 June 2010

Journal Club is held every Friday between 4 Pm-5pm. For change in schedule please check our twitter account or facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

July 13, 2010

Greater risk of dementia when spouse has dementia? The Cache County Study

Filed under: Uncategorized — Tags: , , , — Gogce Crynen @ 9:51 am

New Study Links Marriage and Risk for Dementia A study published in the Journal of the American Geriatric Society reports that spousal caregivers of a dementia patient may have an increased risk for developing dementia themselves. This interesting population based study is the first to empirically explore the effects of caring for a spouse with dementia on caregivers own cognitive status. Results suggest that spouses, particularly male, have a six times greater risk for developing dementia. Prolonged and intense stress may be a major factor in these findings. Norton M, Smith K, Ostbe T et al. Greater risk of dementia when spouse has dementia? The Cache County Study. JAGS 2010; 58:895-900

The Roskamp Institute Memory Clinic and Clinical Trials Division provide a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941) 256-8018.

July 12, 2010

Event: Journal Club “Identification of Caspase-6-Mediated Processing of the Valosin Containing Protein (p97) in Alzheimer’s Disease: A Novel Link to Dysfunction in Ubiquitin Proteasome System-Mediated Protein Degradation”

Chris Mayer will be presenting the paper on Friday (7/16/2010) at Roskamp Institute.

Title: Identification of Caspase-6-Mediated Processing of the Valosin Containing Protein (p97) in Alzheimer’s Disease: A Novel Link to Dysfunction in Ubiquitin Proteasome System-Mediated Protein Degradation

Journal: The Journal of Neuroscience,

April 28, 2010, 30(17):6132-6142

Journal Club is held every Friday between 4 pm-5pm. For change in schedule please check our twitter account or facebook page. Please join us!

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

June 21, 2010

Event: Journal Club “The effect of encapsulated VEGF-secreting cells on brain amyloid load and behavioral impairment in a mouse model of Alzheimer’s disease”

Nowell (Jim) Ganey will be presenting the paper on Friday (6/25/2010) at Roskamp Institute.

Title:The effect of encapsulated VEGF-secreting cells on brain amyloid load and behavioral impairment in a mouse model of Alzheimer’s disease.

Journal : Biomaterials.

2010 Jul;31(21):5608-18. Epub 2010 Apr 28.

Journal Club is held every Friday between 4 Pm-5pm. For change in schedule please check our twitter account or facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949


June 15, 2010

News: FDA advisory committee unanimously recommends approval of Novartis investigational treatment FTY720 to treat relapsing remitting MS

Filed under: news — Tags: , , , , — Gogce Crynen @ 10:11 am

The Roskamp Institute continues to actively recruit clinical research participants for the treatment of both Alzheimer’s disease and Multiple sclerosis. We are proud to share the following press announcement regarding a clinical trial/potential treatment that Roskamp Institute has been involved in since 2006: “FDA advisory committee unanimously recommends approval of Novartis investigational treatment FTY720 to treat relapsing remitting MS“.

The Roskamp Institute Memory Clinic and Clinical Trials Division provide a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941) 256-8018.

June 8, 2010

Event Journal Club:Amyloid-β and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer’s disease mice

Amyloid-β and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer’s disease mice by Rhein et al.

Alex Bishop will be presenting the paper on Friday (6/11/2010) at Roskamp Institute.

Journal Club is held every Friday between 4 Pm-5pm. For change in schedule please check our twitter account or facebook page.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

May 24, 2010

Announcement

Filed under: alzheimer — Tags: , , — Gogce Crynen @ 3:44 pm
The Roskamp Institute Memory Center and Clinical Trials Division is pleased to announce the addition of Ms. Yahdinah Alvarez to the clinical team.  Ms. Alvarez is an experienced clinical trial coordinator with expertise in Alzheimer’s and Parkinson’s disease studies.  If you or your loved one is suffering with Alzheimer’s disease or Parkinson’s disease, please contact the clinic at (941) 256-8018 for information regarding possible treatment options.

The Roskamp Institute Memory Clinic and Clinical Trials Division provide a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941) 256-8018.

May 17, 2010

Do You Or Someone You Care For Suffer From Alzheimer’s Disease?

ALZHEIMER’S DISEASE

A research study is being conducted in our area to evaluate an investigational medication for Alzheimer’s disease.

Qualified participants may receive:

– Study related medical care

– Study medication

– Compensation for time and travel

Please call now for more info:    Dr. Andrew Keegan

941-256-8018 ext. 353

The Roskamp Institute Memory Clinic and Clinical Trials Division provide a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941) 256-8018.

May 14, 2010

Reduction of b-amyloid pathology by celastrol in a transgenic mouse model of Alzheimer’s disease

Filed under: alzheimer — Tags: , , , , — Gogce Crynen @ 9:45 am

By Daniel Paris*, Nowell J Ganey, Vincent Laporte, Nikunj S Patel, David Beaulieu-Abdelahad, Corbin Bachmeier, Amelia March, Ghania Ait-Ghezala, Michael J Mullan published in Journal of Neuroinflammation 2010, 7:17

Abstract

Background: Ab deposits represent a neuropathological hallmark of Alzheimer’s disease (AD). Both soluble and insoluble Ab species are considered to be responsible for initiating the pathological cascade that eventually leads to AD. Therefore, the identification of therapeutic approaches that can lower Ab production or accumulation remains a priority. NFkB has been shown to regulate BACE-1 expression level, the rate limiting enzyme responsible for the production of Ab. We therefore explored whether the known NFkB inhibitor celastrol could represent a suitable compound for decreasing Ab production and accumulation in vivo.

Methods: The effect of celastrol on amyloid precursor protein (APP) processing, Ab production and NFkB

activation was investigated by western blotting and ELISAs using a cell line overexpressing APP. The impact of celastrol on brain Ab accumulation was tested in a transgenic mouse model of AD overexpressing the human APP695sw mutation and the presenilin-1 mutation M146L (Tg PS1/APPsw) by immunostaining and ELISAs. An acute treatment with celastrol was investigated by administering celastrol intraperitoneally at a dosage of 1 mg/Kg in 35 week-old Tg PS1/APPsw for 4 consecutive days. In addition, a chronic treatment (32 days) with celastrol was tested using a matrix-driven delivery pellet system implanted subcutaneously in 5 month-old Tg PS1/APPsw to ensure a continuous daily release of 2.5 mg/Kg of celastrol.

Results: In vitro, celastrol dose dependently prevented NFkB activation and inhibited BACE-1 expression. Celastrol potently inhibited Ab1-40 and Ab1-42 production by reducing the b-cleavage of APP, leading to decreased levels of APP-CTFb and APPsb. In vivo, celastrol appeared to reduce the levels of both soluble and insoluble Ab1-38, Ab1-40 and Ab1-42. In addition, a reduction in Ab plaque burden and microglial activation was observed in the brains of Tg PS1/APPsw following a chronic administration of celastrol.

Conclusions: Overall our data suggest that celastrol is a potent Ab lowering compound that acts as an indirect BACE-1 inhibitor possibly by regulating BACE-1 expression level via an NFkB dependent mechanism. Additional work is required to determine whether chronic administration of celastrol can be safely achieved with cognitive benefits in a transgenic mouse model of AD.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

May 11, 2010

NEWS RELEASE:Investigational Immune Intervention Slows Brain Atrophy in Alzheimer’s Patients


Media Contact:

Cheryl Rindfleisch, Roskamp Institute

941-256-8018 x356

crindfleisch@rfdn.org or

Jeffree Itrich  858-622-5827

jitrich@ucsd.edu

May 10, 2010

Investigational Immune Intervention Slows Brain Atrophy in Alzheimer’s Patients

  • 18-Month Phase 2 Study is First to Show Combined Benefits of IGIV on Clinical Outcomes and Brain-Imaging Measures
  • Phase 3 Study Now Enrolling Participants at the Roskamp Institute in Sarasota

An investigational treatment, Immune Globulin Intravenous (IGIV), which utilizes naturally occurring antibodies in human blood has preserved the thinking abilities of a small group of mild-to-moderate Alzheimer’s patients over 18 months and significantly reduced the rate of brain atrophy. The study was conducted at the New York Presbyterian Hospital/Weill Cornell Medical Center and the results were presented at the American Academy of Neurology (AAN) annual meeting in Toronto in mid-April.

An important next step Phase 3 study of IGIV, called The Gammaglobulin Alzheimer’s Partnership (GAP) Study, is now underway throughout North America. Locally the study is being conducted at the Roskamp Institute in Sarasota, Florida. The Phase 3 study is a prospective, 18-month, randomized, double-blind, placebo-controlled, two dose arm of parallel groups in 360 subjects of both genders, aged 50-89 years old with mild-to-moderate Alzheimer’s disease (AD).

“The cognitive and functional outcomes and neuroimaging results from this 18-month Phase 2 study clearly support continued evaluation for Alzheimer’s disease in a larger number of patients,” says Dr. Paul Aisen, director of the Alzheimer’s’ Disease Cooperative Study at UCSD, one of the study’s sponsors. “The important next step is to fully enroll and complete the ongoing Phase 3 study in hope of confirming the Phase 2 findings and fully understand the potential benefit in AD.”

The Phase 2 study used Gammagard Liquid and Gammagard S/D for Alzheimer’s produced by Baxter Healthcare. The same products are being used in the Phase 3 Gap Study.

“IGIV is being evaluated as a possible treatment for AD because of its known antibodies to beta-amyloid, thought to be the major element of amyloid plaques in the brains of people with AD,” says Dr. Andrew Keegan, the study’s principal investigator at the Roskamp Institute.  “IGIV is not approved for treating AD but is approved in the U.S. and other countries for treating immune deficiency and autoimmune disorders,” he added. “It has been around for a long time and has an excellent safety record.”

Dr. Norman Relkin, director of the Memory Disorders Program at New York Presbyterian Hospital/Weill Cornell Medical Center and principal investigator of the Phase 2 study reported at the AAN that patients who received IGIV once or twice a month for 18 months had significantly lower rates of ventricular enlargement (6.7% vs 12.7% per year) and less whole brain atrophy (1.6% vs 2.2% per year) than control subjects who initially received the placebo. Relkin’s findings were based on two independent analyses of brain-imaging data from 20 patients who underwent serial MRI scans during the Phase 2 study of IGIV for Alzheimer’s disease (AD).

The brain of a typical AD patient shrinks three to four times faster than a healthy equivalent older adult due to the accelerated brain cell death. Shrinkage of brain tissue causes the fluid-filled ventricles at the brain’s center to enlarge at a faster rate than normal. Changes in the size of the brain and ventricles can be measured accurately by analyzing results from two or more MRI scans at intervals of several months apart. The unprecedented reductions in these measures after IGIV was administered in the Phase 2 study may indicate that IGIV exerts a disease-modifying effect that the current generation of AD treatments do not. Relkin found that rates of brain shrinkage were independent of the subject’s age, gender and brain volume at the beginning of the study but strongly correlated with IGIV dose and the clinical outcomes after 18 months of intervention. The research team also found that patients who responded best to IGIV did not measurably decline over 18 months, plus had an average rate of brain shrinkage and average rate of ventricular enlargement comparable to the rate of normal elderly adults.

“A dose related effect of an Alzheimer’s intervention on brain ventricular enlargement has never been seen before, and it suggests that IGIV may be sparing brain tissue,” says Dr. James Brewer, a neurologist and assistant professor in the neurosciences department at UCSD.

Dr. Diamanto Tsakanikas, a neuropsychologist at Presbyterian Hospital/Weill Cornell Medical Center conducted cognitive testing of the Phase 2 study participants while blinded to whether the patients received IGIV or placebo. Her testing revealed that AD patients who received uninterrupted IGIV for 18 months showed significantly less decline in their overall function and thinking abilities than AD patients who were initially given the placebo.

The pivotal Phase 3 study now underway at the Roskamp Institute is funded by Baxter and National Institutes of Health (NIH) through the Alzheimer’s Disease Cooperative Study (ADCS).

The Phase 2 study was supported by Baxter Healthcare, the Citigroup Foundation and The Clinical Translational Science Center of Weill Cornell Medical College.

For further information on the Phase 3 study go to www.GAPSTUDY.com or http://www.alzheimers.org/clinicaltrials/fullrec.asp?PrimaryKey=282 .

Local Site:

Roskamp Institute

(941) 256-8018

www.rfdn.org

May 10, 2010

Journal Club

Filed under: alzheimer — Tags: , , — Gogce Crynen @ 11:02 am

Jeremy Frieling is presenting “Days-to-criterion as an indicator of toxicity associated with human Alzheimer amyloid- oligomers” by Gandy et al.

Location: Roskamp Institute

Date: May 14th 2010

Time: 4:00PM

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

May 7, 2010

FREE MEMORY SCREENING-Sarasota FL

Filed under: alzheimer — Tags: , , , , — Gogce Crynen @ 1:40 pm

Are you or someone you know suffering from memory loss or forgetfulness?

Roskamp Institute is offering FREE MEMORY SCREENING for adults age 60 or older.

For an appointment call:               Roskamp Institute

941-256-8018 ext. 349


The Roskamp Institute Memory Clinic and Clinical Trials Division provide a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941) 256-8018.

May 6, 2010

Anti-Tumoral Activity of a Short Decapeptide Fragment of the Alzheimer’s Abeta Peptide

By Daniel Paris • Nikunj Patel • Nowell J. Ganey • Vincent Laporte • Amita Quadros • Michael J. Mullan

Int J Pept Res Ther (2010) 16:23–3.  DOI 10.1007/s10989-010-9198-8

Abstract: The inhibition of angiogenesis is regarded as a promising avenue for cancer treatment. Although some antiangiogenic compounds are in the process of development and testing, these often prove ineffective in vivo, therefore the search for new inhibitors is critical. We have recently identified a ten amino acid fragment of the Alzheimer Ab peptide that is anti-angiogenic both in vitro and in vivo. In the present study, we investigated the antitumoral potential of this decapeptide using human MCF-7 breast carcinoma xenografts in nude mice. We observed that this decapeptide was able to suppress MCF-7 tumor growth more potently than the antiestrogen tamoxifen. Inhibition of tumor vascularization as determined by PECAM-1 immunostaining and decreased tumor cell  proliferation as determined by Ki67 immunostaining were observed following treatment with the Ab fragment. In vitro, this peptide had no direct impact on MCF-7 tumor cell proliferation and survival suggesting that the inhibition of tumor growth and tumor cell proliferation observed in vivo is related to the antiangiogenic activity of the peptide. Taken together these data suggest that this short Ab derivative peptide may constitute a new antitumoral agent.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

May 5, 2010

Diagnostic utility of APOE, soluble CD40, CD40L, and Abeta1-40 levels in plasma in Alzheimer’s disease

Filed under: cd40 — Tags: , , , , , , — Gogce Crynen @ 9:36 am

By Ait-ghezala G, Abdullah L, Volmar CH, Paris D, Luis CA, Quadros A, Mouzon B, Mullan MA, Keegan AP, Parrish J, Crawford FC, Mathura VS, Mullan MJ.

Cytokine. 2008 Nov;44(2):283-7.

A continuous inflammatory state is associated with Alzheimer’s disease (AD) evidenced by an increase in proinflammatory cytokines around beta-amyloid (Abeta) deposits. In addition, functional loss of CD40L is shown to result in diminished Amyloid precursor proton (APP) processing and microglial activation, supporting a prominent role of CD40-CD40L in AD etiology. We therefore hypothesize that a peripheral increase in Abeta may result in corresponding increase of sCD40 and sCD40L further contributing to AD pathogenesis. We measured plasma Abeta, sCD40 and sCD40L levels in 73 AD patients and compared to 102 controls matched on general demographics. We demonstrated that Abeta(1-40), levels of sCD40 and sCD40L are increased in AD and declining MMSE scores correlated with increasing sCD40L, which in turn, correlated positively with Abeta(1-42). We then combined sCD40, sCD40L, Abeta and APOE and found that this biomarker panel has high sensitivity and specificity (>90%) as a predictor of clinical AD diagnosis. Given the imminent availability of potentially disease modifying therapies for AD, a great need exists for peripheral diagnostic markers of AD. Thus, we present preliminary evidence for potential usefulness for combination of plasma sCD40, sCD40L along with Abeta(1-40) and APOE epsilon4 in improving the clinical diagnosis of AD.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

May 3, 2010

CD40/CD40L interaction induces Abeta production and increases gamma-secretase activity independently of tumor necrosis factor receptor associated factor (TRAF) signaling.

Filed under: cd40 — Tags: , , , , — Gogce Crynen @ 4:53 pm

By Volmar CH, Ait-Ghezala G, Frieling J, Weeks OI, Mullan MJ.

Exp Cell Res. 2009 Aug 1;315(13):2265-74.

CD40, a member of tumor necrosis factor receptor superfamily, and its cognate ligand CD40L are both elevated in the brain of Alzheimer’s disease (AD) patients compared to controls. We have shown that pharmacological or genetic interruption of CD40/CD40L interaction results in mitigation of AD-like pathology in vivo in transgenic AD mouse models, and in vitro. Recently, we showed that CD40L stimulation could increase Abeta levels via NFkappaB signaling, presumably through TRAFs. In the present work, using CD40 mutants, we show that CD40L can increase levels of Abeta(1-40), Abeta(1-42), sAPPbeta, sAPPalpha and CTFbeta independently of TRAF signaling. We report an increase in mature/immature APP ratio after CD40L treatment of CD40wt and CD40-mutant cells, reflecting alterations in APP trafficking. In addition, results from CD40L treatment of a neuroblastoma cell line over-expressing the C-99 APP fragment suggest that CD40L has an effect on gamma-secretase. Furthermore, inhibition of gamma-secretase activity significantly reduces sAPPbeta levels in the CD40L treated HEK/APPsw CD40wt and the CD40-mutant cells. The latter suggests CD40/CD40L interaction primarily acts on gamma-secretase and affects beta-secretase via a positive feedback mechanism. Taken together, our data suggest that CD40/CD40L interaction modulates APP processing independently of TRAF signaling.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

April 30, 2010

Roskamp Institute Poster Abstract from VA Reasearch Week

Filed under: Uncategorized — Tags: , , , , , , , , — Gogce Crynen @ 10:22 am

As I mentioned before, most of the PhD students and research assistants from our Institute participated in poster session  that was organized as a part of VA Research Week event series. Here you will find the abstract of our posters, enjoy :)

Development of the Barnes Maze as an Alternative to the Morris Water Maze Following TBI in Mice.

Scott Ferguson1,2, Benoit Mouzon1,2, John Phillips1, Vani Ganapapthi1, Alex Bishop1, Gogce Kayihan1,2, Venkatarajan Mathura1,2, Michael Mullan1,2 , Fiona Crawford1,2

1The Roskamp Institute, Sarasota, FL, USA; 2 James A Haley Veterans Administration, Tampa, FL, USA

Traumatic brain injury (TBI) is suffered by approximately 1.4 million people in the United States each year. TBI is the leading cause of death and disability in the most active population (under 45 years of age) in industrialized countries. Within the military, TBI is associated with 59% of blast-associated injuries seen at Walter Reed Army Medical Center, and between January 2003 and May 2005, 31% of all admissions to WRAMC had a brain injury. Apolipoprotein E (APOE) polymorphisms are known to impact the outcome after TBI, with the APOE4 allele (and concomitant ApoE4 expressed protein) associated with worse outcome than ApoE3 following TBI.   As part of our TBI research program we are exploring the molecular, neurobehavioral and neuropathological outcome after TBI in mouse models of injury, including APOE transgenic mice.

In order to evaluate differential outcomes of injury and its effects on motor skills and memory, we have optimized a series of neurobehavioral tests in mice.  The Rotarod test measures motor skill and learning via a programmable rotating bar.  Rotarod has shown the ability to distinguish between injured and uninjured mice, and has shown appropriate trends between differing levels of injury.  Morris water maze is a test of spatial memory and learning originally designed for rats but later adapted for mice.  APOE3 mice performed better than APOE4 mice in our Rotarod results, demonstrating an APOE genotype-dependent effect on motor function following TBI.  However, in the cognitive paradigm not only did we fail to detect any APOE genotype-dependent effects, we observed no significant differences in performance between injured and uninjured mice.  We therefore explored other cognitive paradigms for their ability to discriminate between injured and uninjured mice.

The Barnes maze is analogous to the Morris water maze in that it is also a test of spatial memory and learning, but because swimming is not involved it is associated with less stress than MWM typically induces in mice.  Others have shown that there is a strain-dependent effect on the ability of mice to learn the water maze task as well as the Barnes maze task.  Given that C57BL/6J mice are reported to perform better on the Barnes maze task, and this is the background strain utilized in our research, we optimized a paradigm of the Barnes maze for use in our TBI studies.  Our results show a statistically significant effect of injury on the spatial memory and learning of C57BL/6J wild type mice.  Future studies will re-examine the effect of APOE genotype on spatial memory following TBI using this test.

This research was funded by a Department of Defense award (W81XWH-07-1-0700) to Dr. Fiona Crawford and by the Roskamp Foundation

APP is Internalized After CD40 Ligation Which Increases Aβ Production

Ghania Ait-Ghezala, Jeremy Frieling, Myles Mullan, Claude-Henry Volmar, and Michael J. Mullan.

CD40, a member of the tumor necrosis factor receptor superfamily, and its cognate ligand CD40L are both elevated in the brains of Alzheimer’s disease (AD) patients compared to controls. We have shown that pharmacological or genetic interruption of CD40/CD40L interaction results in mitigation of AD-like pathology in vivo in transgenic AD mouse models, and in vitro. Recently, we showed that CD40L stimulation could increase Aβ levels, but the mechanism causing this phenomenon is not known. Here we show that CD40 ligation triggers internalization of APP and that internalization by endocytosis is associated with increased Aβ production. Furthermore, anthocyanins, which are known to impact trafficking to and from lipid rafts, impair the production of Aβ by CD40L stimulated CD40. However, anthocyanins have no effect on CD40L treatment of a neuroblastoma cell line over-expressing the C-99 APP fragment suggesting that CD40L internalization has no effect on γ-secretase. This finding is consistent with previous data suggesting that endocytosis increases BACE activity. In summary, these data suggest that a general mechanism of increased Aβ generation may be lipid raft mediated internalization of APP allowing increased BACE activity on its substrate.

Neurobehavioral profiles of two mouse models of Gulf War Illness

Laila Abdullah1, Alex Bishop1, John Phillips1, Benoit Mouzon1,2, Scott Ferguson1,2, Vani Ganapathi1, Myles Mullan1,2, Ghania Ait-Ghezala PhD1,2, Michael Mullan MD, PhD1,2 and Fiona Crawford PhD1,2

Affiliations: 1Roskamp Institute, 2040 Whitfield Ave, Sarasota, FL, 34243, 2James A. Haley VA Hospital, 13000 Bruce B. Downs Blvd, Tampa, FL, 33612.

Background: Gulf War Illness (GWI) is a multisymptom condition associated with service in the 1990-1991 Persian Gulf War conflict and affects around 250,000 US veterans. It is largely attributed to combined exposure to pyridostigmine bromide (PB) and overuse of pesticides and insect repellants.  After nearly two decades, there is still no treatment for GWI and the underlying pathologic factors associated with the observed central nervous system (CNS)-based symptoms in veterans remain unclear.  Current GWI animal models do not demonstrate the full spectrum of neurobehavioral features reported to be associated with GWI, which makes it particularly difficult to explore the efficacy of possible therapeutic options.  Therefore, we tested two different treatment paradigms in order to establish a mouse model of GWI, which exhibits motor, cognitive and anxiety-related symptoms that are observed in veterans with this illness.  Methods: For model A, a previously established treatment paradigm was used which showed pathological changes suggestive of neurodegeneration, however extensive neurobehavioral profiling was not performed. Treated C57BL6 mice received oral administration of 1.3mg/kg of PB in water, dermal application of 0.13mg/kg of permethrin (PER) and 40 mg/kg of N-N-diethyl m-toluamide 2 (DEET) in 70% ethanol and 5 minutes of restrained stress daily for 28 days, whereas control mice received vehicle for the same duration.  For model B, a new treatment paradigm was developed where CD1 mice in the treatment group were administered 2mg/kg of PB and 200 mg/kg of PER via i.p. in DMSO daily for 10 days and the control group received DMSO only.  Following treatment, neurobehavioral profiles were examined using the Rotarod test to assess motor deficits, the Open Field test for anxiety-related changes and the Morris Water Maze test to assess spatial memory.  Results: In model A, treatment was associated with significant impairment in sensorimotor function and presence of anxiety-related behavior, but there was no deficit in spatial memory.  In model B, a delayed adverse effect of treatment was observed on the outcome measures of anxiety and spatial memory, but there was no evidence of sensorimotor impairment.  Conclusion: These findings suggest that combined exposure to PB and pesticides/insect repellents may lead to CNS-based effects in mice that mimic some of the clinical symptoms observed in veterans with GWI.  Additional studies are required to determine whether all three neurobehavioral features can be produced in one mouse model and whether these changes correlate with pathological features associated with neurodegeneration.

Acknowledgment: Funding for this research is provided by a Congressionally Directed Medical Research award (GW080094) to Dr. Fiona Crawford.

Proteomic identification of plasma TBI biomarkers

Benoit Mouzon1,2, Alex Bishop1, Gogce Kayihan1,2, Ben Katz1, Scott Ferguson1,2, Jon Reed1, Venkatarajan Mathura1, Michael Mullan1,2 and Fiona Crawford1,2

1Roskamp Institute, Sarasota, Florida

2James A. Haley Veterans’ Hospital, Tampa, Florida

Traumatic Brain Injury (TBI) is a major cause of mortality and morbidity in both military and civilian populations. The current lack of prognostic biomarkers for TBI confounds treatment and management of patients and is of increasing concern as the TBI population grows.  As part of our TBI research program we are generating brain and plasma proteomic profiles from APOE3 and APOE4 transgenic mice which demonstrate relatively favorable and unfavorable outcomes respectively, following TBI.  In this study we used proteomic approaches to identify the changes in plasma protein profiles in APOE3 and APOE4 mice following severe TBI, in order to determine peripheral biomarkers associated with a poor outcome after TBI.

Using a quantitative proteomics approach (isobaric tagging for relative and absolute quantitation – iTRAQ) we have identified proteins that are significantly modulated as a function of APOE genotype, injury and the interactive term of “genotype*injury”. Analysis of modulated plasma proteins revealed significant differences in proteomic response at 24 hours, 1 month and 3 months post injury across genotypes.  From these proteomic datasets we have identified 83 proteins at the 24 hour timepoint, 170 at 1 month and 129 at 3 months post TBI. For each timepoint, the identified proteins included those whose response was dependent on injury or the injury*genotype interaction, suggesting them as potential biomarkers of injury or outcome following injury.

In pilot validation studies, using antibody-based approaches in the original plasma from these mice, we have demonstrated the validity of our approach.  These preliminary data clearly demonstrate plasma protein changes that are not only injury-dependent but also interaction-dependent. The identified proteins include biomarkers that have been previously implicated in human TBI, and their time course and relationship to neurobehavior and pathology are now to be examined in these mouse models.  Importantly these results demonstrate the presence of TBI-dependent and interaction-dependent plasma proteins at a 3 months time point, which is a considerable time post-injury in the mouse model and will potentially be of significance for combat veterans receiving assessment at extended periods post-injury.  Furthermore, our identification of clusters of related proteins indicates disturbance of particular biological modules which increases their value beyond that of solitary biomarkers.  Clinical assays for many of these proteins are already established, which will facilitate translation of our findings from mouse to human.

The biomarker panels developed from this work will aid clinicians in the determination of diagnosis, prognosis, appropriate treatment and monitoring response to treatment, all of which are urgently needed in TBI management. The next step will be to investigate these potential biomarkers in human TBI patients and those studies will begin this year with the VA patient population and our clinical collaborators.

Acknowledgement:  This research was funded by a Department of Defense award (W81XWH-07-1-0700) to Dr. Fiona Crawford.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949


April 27, 2010

High serum Abeta and vascular risk factors in first-degree relatives of Alzheimer’s disease patients

By Abdullah L, Luis C, Paris D, Ait-ghezala G, Mouzon B, Allen E, Parrish J, Mullan MA, Ferguson S, Wood M, Crawford F, Mullan M. These findings were published in Molecular Medicine 2009 Mar-Apr;15(3-4):95-100.

Alzheimer’s disease is clinically characterized by progressive cognitive decline accompanied by the presence of amyloid plaques and neurofibrillary tangles in the brain of Alzheimer’s patients. A small protein fragment beta-amyloid (Abeta) with 42 amino acids is shown to deposit earlier in the disease process than the slightly shorter form (40 amino acid fragment).  Both species of this protein fragment are considered toxic to the brain and are shown to have an important role in causing Alzheimer’s disease.  Current research suggests that the disease process in Alzheimer’s begins long before the presence of palpable symptoms and widespread damage in the brain. Therefore, use of beta-amyloid seems promising in identification of individuals at-risk of developing Alzheimer’s disease.  Clinical studies have previously shown that blood and cerebrospinal fluid levels of Abeta may be helpful in diagnosis of Alzheimer’s disease but are influenced by factors such as presence of family history and other risk factors. The main objective of a recent study published by the scientists at the Roskamp Institute was to determine whether elevated blood Abeta levels among the first-degree relatives of patients with Alzheimer’s disease are associated with certain risk factors of cardiovascular disease that are also risk factors Alzheimer’s disease, such as hypertension.  Blood Abeta was measured in disease-free first-degree relatives of patients with Alzheimer-like dementia. Study participants were recruited as part of an ancillary study of the Alzheimer’s Disease Anti-inflammatory Prevention Trial (ADAPT subpopulation) which was funded by the National Institutes of Health (UO1AG15477).  Examination of Abeta in this group of individuals showed that Abeta(1-40) fragment was positively associated with age and use of anti-hypertensive medications, but a negative relationship was observed in those individuals who experienced some increase in systolic blood pressure, despite being on anti-hypertensive medication.  On the other hand, the more toxic Abeta(1-42) was associated with statin use (medications used for lowering cholesterol) and with high-density lipoproteins was observed among statin nonusers. These findings suggest that high Abeta in blood samples of family history-enriched individuals may be due to enrichment of vascular risk factors and may reflect presymptomatic stage of Alzheimer’s disease.  As anti-hypertensive medications and statins are considered to be protective against Alzheimer’s disease onset, it remains to be determined whether their association with Abeta reflects mitigation of Abeta-related toxicity in the brain. Longitudinal evaluation of blood Abeta in this cohort will provide a better understanding of the significance of this association in Alzheimer’s disease etiology.

The Roskamp Institute is devoted to understanding causes and finding cures for neuropsychiatric and neurodegenerative disorders and addictions. The Institute utilizes a broad range of scientific approaches to understanding the causes of and potential therapies for these disorders with an emphasis on Alzheimer’s disease. For more information, please call (941)752-2949

April 26, 2010

Journal Club: The presence of sodium dodecyl sulphate-stable Aβ dimers is strongly associated with Alzheimer-type dementia

Filed under: Uncategorized — Tags: , , , — Gogce Crynen @ 11:13 am

JC Nowell Ganey will present “The presence of sodium dodecyl sulphate-stable Aβ dimers is strongly associated with Alzheimer-type dementia” on Thursday (29th April 2010) at 4:00pm in Roskamp Institute. You can find the article in the following link.

The Roskamp Institute provides a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941)752-2949

Alzheimer’s Disease Anti-Inflammatory Prevention Trial

The Roskamp Institute Memory Center is actively following a large number of subjects who participated in the Alzheimer’s Disease Anti-Inflammatory Prevention Trial (ADAPT). Although earlier detection and the development of disease modifying treatment continues to be a primary focus of research and several potential compounds are under clinical trial, more prevention studies are needed.

The Roskamp Institute provides a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941) 256-8018.

April 23, 2010

Reduction of β-amyloid pathology by celastrol in a transgenic mouse model of Alzheimer’s disease

Filed under: alzheimer — Tags: , , — admin @ 2:59 pm

Daniel Paris email, Nowell J Ganey email, Vincent Laporte email, Nikunj S Patel email, David Beaulieu-Abdelahad email, Corbin Bachmeier email, Amelia March email, Ghania Ait-Ghezala email and Michael J Mullan email

The Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA

author email corresponding author email

Journal of Neuroinflammation 2010, 7:17doi:10.1186/1742-2094-7-17
Published: 8 March 2010
Abstract
Background

Aβ deposits represent a neuropathological hallmark of Alzheimer’s disease (AD). Both soluble and insoluble Aβ species are considered to be responsible for initiating the pathological cascade that eventually leads to AD. Therefore, the identification of therapeutic approaches that can lower Aβ production or accumulation remains a priority. NFκB has been shown to regulate BACE-1 expression level, the rate limiting enzyme responsible for the production of Aβ. We therefore explored whether the known NFκB inhibitor celastrol could represent a suitable compound for decreasing Aβ production and accumulation in vivo.
Methods

The effect of celastrol on amyloid precursor protein (APP) processing, Aβ production and NFκB activation was investigated by western blotting and ELISAs using a cell line overexpressing APP. The impact of celastrol on brain Aβ accumulation was tested in a transgenic mouse model of AD overexpressing the human APP695sw mutation and the presenilin-1 mutation M146L (Tg PS1/APPsw) by immunostaining and ELISAs. An acute treatment with celastrol was investigated by administering celastrol intraperitoneally at a dosage of 1 mg/Kg in 35 week-old Tg PS1/APPsw for 4 consecutive days. In addition, a chronic treatment (32 days) with celastrol was tested using a matrix-driven delivery pellet system implanted subcutaneously in 5 month-old Tg PS1/APPsw to ensure a continuous daily release of 2.5 mg/Kg of celastrol.
Results

In vitro, celastrol dose dependently prevented NFκB activation and inhibited BACE-1 expression. Celastrol potently inhibited Aβ1-40 and Aβ1-42 production by reducing the β-cleavage of APP, leading to decreased levels of APP-CTFβ and APPsβ. In vivo, celastrol appeared to reduce the levels of both soluble and insoluble Aβ1-38, Aβ1-40 and Aβ1-42. In addition, a reduction in Aβ plaque burden and microglial activation was observed in the brains of Tg PS1/APPsw following a chronic administration of celastrol.
Conclusions

Overall our data suggest that celastrol is a potent Aβ lowering compound that acts as an indirect BACE-1 inhibitor possibly by regulating BACE-1 expression level via an NFκB dependent mechanism. Additional work is required to determine whether chronic administration of celastrol can be safely achieved with cognitive benefits in a transgenic mouse model of AD.

April 22, 2010

Volunteers for early detection of cognitive decline in older adults

Dr. Cheryl Luis of the Roskamp Institute was awarded a New Investigator Research Grant from the Alzheimer’s Association in 2009.  She is studying the potential usefulness of a blood test in combination with a paper and pencil memory test for early detection of cognitive decline in older adults.  Additional research volunteers are needed.  If you or your loved one has been diagnosed with Alzheimer’s disease or Mild Cognitive Impairment and are interested in participating in a brief study, please call (941) 256-8018

The Roskamp Institute provides a full range of services for individuals with Alzheimer’s disease including diagnostic work-up and follow-up treatment, neuropsychological examination, clinical trial opportunities, and memory screening.  For more information, please call (941) 256-8018.

September 10, 2009

World Alzheimer’s Day: Leaders Call for Early Diagnosis and Aggressive Research

Filed under: Uncategorized — Tags: , , — admin @ 9:59 am

Alzheimer’s disease carries an annual price tag of $148 billion dollars, not to mention the personal toll that it takes on the over 5.3 million patients and their families.

More than 5.3 million Americans are living with Alzheimer’s, and every 72 seconds someone in America develops the disease. According to the Alzheimer’s Association, by mid-century someone will develop Alzheimer’s every 33 seconds, and there will be nearly a million new cases per year.

“With the country facing unprecedented economic challenges and a rapidly aging baby boomer population, now is the time to address the burgeoning Alzheimer’s crisis that triples healthcare costs for Americans aged 65 and over,” said Harry Johns, Alzheimer’s Association CEO.

Alzheimer’s disease is a neurodegenerative disorder characterized by progressive loss of memory and cognitive function. It destroys brain cells, causing problems with memory, thinking, and behavior that are severe enough to affect everyday life.

Experts believe that early detection of Alzheimer’s disease and early intervention with improved therapies provides the greatest opportunity to modify or halt disease progression. Most current therapies for Alzheimer’s treat the symptoms associated with it and not the disease itself.

“There is a rich, diverse variety of treatment possibilities for Alzheimer’s that scientists are exploring, offering great hope that drugs that may slow or even reverse disease progression could be on the horizon—saving millions of dollars in public health programs,” said Ronald Petersen, M.D., Ph.D, Alzheimer’s Association Medical Scientific Advisory Council Chair. On World Alzheimer’s Day, we renew our commitment to early diagnosis and aggressive Alzheimer’s research in order to improve the health outcomes for people living with this disease.

Dr. Andrew Keegan and other local physicians are currently researching potential new treatments for Alzheimer’s patients that target causes of the disease, such as amyloid plaques in the brain. The buildup of these plaques is thought to cause Alzheimer’s disease. Some of these investigational drugs use antibodies, or immune system proteins, to dissolve the plaques.

“There are too many lives, too little time, and too much at stake for anything less than an aggressive plan to address the threat of this disease,” Johns said.

Roskamp is a not-for-profit research Institute located in Sarasota, Fla., that is dedicated to understanding the causes of, and finding cures for, neuropsychiatric and neurodegenerative disorders with an emphasis on Alzheimer’s disease. The Institute’s Memory Clinic also offers comprehensive cognitive and medical assessment toward differential diagnosis of Alzheimer’s disease and offers treatments and disease management options once the diagnostic evaluation is complete.

Contact:
Dr. Andrew Keegan
Roskamp Institute
email: rclinic @ rfdn.org
Phone: (941)256-8018
www.RoskampInstitute.com

For more information, please contact the Institute at (941) 752-2949, Roskamp’s Clinical Trials Division in Sarasota at (941) 256-8018 or visit www.RoskampInstitute.com.

August 11, 2009

Dementia in Older Women

Filed under: Uncategorized — Tags: , , — admin @ 1:13 pm

A recent paper published in the Journal Neurology, which analyzed over 900 people, suggests that almost half of all women in their nineties are suffering from dementia. The study carried out in California is one of a few looking specifically at the rates of dementia in the very old. However, given our increased life expectancies, the over ninety group is growing rapidly in many populations, including that of the United States. Importantly, there seems to be a sex difference in the risk for Alzheimer’s or dementia in general over the age of ninety.

In men, for instance, although there was an increase in the likelihood of having dementia over the age of ninety, it did not increase as much as it did in women. In women, the likelihood of having dementia doubled every five years after the age of ninety. Previous studies have suggested that the risk for dementia is higher in women than it is in men. But other studies have disputed this. This present study seems to confirm that the risk for women is greater than men, at least after the age of ninety years.

Therefore, if you divide dementia populations by sex over the age of ninety, about 45% of women will have dementia compared to 28% of men. Importantly the study also suggested that women who had used their brains (intellect) more throughout life and had achieved higher education, were much less likely to develop dementia than those who had not.

Understanding why women in this age group might be at higher risk will take additional studies. But it is known, for instance, that women are more likely than men to develop stroke and heart disease as they age. Both of these are independent risk factors for dementia and exacerbate Alzheimer’s symptoms.

Researchers at the Roskamp Institute are interested in finding new treatments for Alzheimer’s disease and clues from sex differences that confer different risks for Alzheimer’s are important because they may point to more treatment strategies.

Researchers have, for instance, speculated that estrogen is a protective factor for Alzheimer’s disease, but proactive treatment with estrogen has not been shown to be preventative in clinical trials. In the present study, the idea that vascular risk factors (which are more prevalent in women as they age) are contributory to Alzheimer’s is consistent with much of the work of Roskamp Institute scientists showing that in the presence of amyloid, damage to the vasculature is heightened and the consequences of vascular damage has greater impact on the brain in the presence of early Alzheimer’s disease than in normal individuals. These and other clues are leading Roskamp Institute scientists towards new treatments for the disease, some of which should be entering clinical trials in 2008.

NSAIDS and their effect on Alzheimers disease

Filed under: Uncategorized — Tags: , , — admin @ 12:45 pm

Non-steroidal anti-inflammatory (NSAIDS) drugs such as Naproxen and Celecoxib do not improve cognition in at-risk older adults. These findings from the Alzheimer’s Disease Anti-Inflammatory Prevention Trial (ADAPT) were published this month in Archives of Neurology.  The Roskamp Institute Memory Clinic in Tampa was one of a handful of centers across the United States that took part in this primary prevention trial funded by the National Institute of Aging. The Tampa site enrolled over 400 subjects, age 70 or older with a reported family history of Alzheimer’s-like dementia.  During the 5-year study period, participants underwent annual cognitive testing and were randomly assigned to one of two treatments (Naproxen 220 mg twice daily, Celecoxib 220 mg twice daily) or a placebo. Although treatment was suspended in 2004, following a report of increased cardiovascular risk in another prevention trial, subjects continued annual follow-up.  Results examining the cognitive data collected up to 6 months after treatment was discontinued suggest that Naproxen may in fact have a small deleterious effect on cognition. However further study is needed to determine if this effect is mitigated or exaggerated over time, or if results were influenced by subjects who may have been in the early stage of a dementia. Drs. Cheryl Luis and Timothy Crowell, specialists in Neuropsychology, supervised the day-to-day aspects of the study in Tampa. Dr. Michael Mullan, director of the Roskamp Institute and principal investigator for the Tampa site served on the writing committee of the manuscript. Go to http://www.ncbi.nlm.nih.gov/pubmed/18474729 for more information.

    Keywords:
  • alzheimers disease
  • alzheimers disease assessment scale
  • alzheimers disease end stage
  • alzheimers disease symptoms
  • symptoms of alzheimers disease
  • alzheimers disease and
  • alzheimers disease articles
  • alzheimers disease care
  • alzheimers disease diagnosis
  • alzheimers disease fact
  • alzheimers disease help
  • alzheimers disease info
  • alzheimers disease information
  • alzheimers disease photos
  • alzheimers disease picture
  • alzheimers disease stage
  • alzheimers disease statistics
  • alzheimers disease support
  • alzheimers disease test
  • alzheimers disease type
  • dementia alzheimers disease
  • information on alzheimers disease
  • prevent alzheimers disease
  • symptom of alzheimers disease
  • treatment for alzheimers disease
  • alzheimer’s disease statistics
  • alzheimer’s disease assessment
  • alzheimer’s disease
  • early onset alzheimer’s disease
  • what is alzheimer’s disease
  • alzheimer’s disease assessment scale
  • alzheimer’s disease information
  • information on alzheimer’s disease
  • alzheimer’s disease articles
  • alzheimer’s disease drug
  • alzheimer’s disease and dementia
  • alzheimer’s disease diagnosis
  • alzheimer’s disease info
  • alzheimer’s disease treatment
  • alzheimer’s disease treatments
  • causes of alzheimer’s disease
  • stages of alzheimers
  • signs of alzheimers
  • stage of alzheimers
  • early signs of alzheimers
  • sign of alzheimers
  • brain injury
  • mild brain injury
  • traumatic brain injury
  • mild traumatic brain injury
  • trumatic brain injury
  • beta amyloid
  • beta amyloid antibody
  • anti beta amyloid antibodies
  • anti beta amyloid antibody
  • beta amyloid antibodies
  • alzheimers
  • alzheimers association
  • what is alzheimers
  • diagnosing alzheimers
  • dementia vs alzheimers
  • aluminum alzheimers
  • information on alzheimers
  • alzheimers donation
  • alzheimers memory walk
  • aids alzheimers
  • alzheimers assoc
  • alzheimers com
  • alzheimers desease
  • alzheimers picture
  • alzheimers signs
  • alzheimers test
  • alzheimers testing
  • alzheimers treatments
  • alzheimers walk
  • early alzheimers
  • end stage alzheimers
  • familial alzheimers
  • alzheimers activity
  • alzheimers and parkinsons disease
  • alzheimers bracelet
  • alzheimers brain disease
  • alzheimers drug treatment
  • alzheimers drugs
  • alzheimers help
  • alzheimers information
  • alzheimers organization
  • alzheimers patients
  • alzheimers screening
  • alzheimers store
  • alzheimers symptom
  • alzheimers symptoms
  • book on alzheimers
  • cure for alzheimers
  • alzheimer s disease
  • amyloid disease
  • alzheimer disease
  • cardiovascular disease
  • disease
  • vascular disease
  • celiac disease
  • coronary artery disease
  • disease symptoms
  • dementia disease
  • parkinson disease
  • parkinsons disease
  • alzheimer disease history
  • blood disease
  • crohns disease
  • stages alzheimer disease
  • about alzheimer’s
  • alzheimer’s association
  • alzheimer’s info
  • alzheimer’s information
  • alzheimer’s statistics
  • alzheimer’s treatments
  • coping with alzheimer’s
  • activities for alzheimer’s patients
  • alzheimer’s activities
  • alzheimer’s research
  • alzheimer’s society
  • alzheimer’s stages
  • alzheimer’s symptoms
  • early signs of alzheimer’s
  • alzheimer’s treatment
  • early onset alzheimer’s
  • treatment for alzheimer’s
  • treatments for alzheimer’s
  • what is alzheimer’s
  • alzheimer’s
  • alzheimer’s stages of
  • alzheimer’s diagnosis
  • alzheimer’s diseases
  • information on alzheimer’s
  • alzheimer’s bracelet
  • alzheimer’s care facilities
  • alzheimer’s caregivers
  • alzheimer’s cure
  • alzheimer’s drugs
  • alzheimer’s news
  • alzheimer’s signs
  • alzheimer’s support
  • alzheimer’s support groups
  • alzheimer’s test
  • alzheimer’s therapy
  • alzheimer treatment
  • alzheimer treatments
  • alzheimer society
  • what is alzheimer
  • alzheimer
  • alzheimer s
  • alzheimer association
  • alzheimer symptoms
  • alzheimer test
  • activities for alzheimer
  • activities for alzheimer patients
  • alzheimer care
  • alzheimer diagnosis
  • alzheimer foundation
  • alzheimer information
  • alzheimer research
  • alzheimer support groups
  • early onset alzheimer
  • dementia
  • dementia activities
  • dementia stages
  • dementia care
  • dementia symptoms
  • symptoms of dementia
  • what is dementia
  • vascular dementia
  • dementia support
  • early dementia
  • frontal lobe dementia
  • lewy body dementia
  • stages of dementia
  • dementia research
  • early onset dementia
  • elderly dementia
  • senile dementia
  • amyloidosis
  • head trauma
  • roskamp institute
  • brain injuries
  • amyloid
  • diseases
  • head injuries
  • brain stem injury
  • cardiovascular diseases
  • head injury
  • closed head injury
  • amyloid antibody
  • roskamp
  • amyloid antibodies
  • amyloid diseases
  • brain tumor
  • brain trauma

Powered by WordPress