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Roskamp Institute Articles Better Science. Real Discovery.

March 15, 2012

Event: Journal Club ” Multicolor time-stamp reveals the dynamics and toxicity of amyloid deposition “

Filed under: Uncategorized — Tags: , , , — Gogce Crynen @ 12:45 pm

Chris Mayer will be presenting the paper on Friday (3/16/2012) at 4:00 PM in Roskamp Institute. Title:  ” Multicolor time-stamp reveals the dynamics and toxicity of amyloid deposition”

Condello C.,  Schain A., Grutzendler J. Multicolor time-stamp reveals the dynamics and toxicity of amyloid deposition. 2011. Scientific Reports 1, Article number: 19 doi:10.1038/srep00019

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 9, 2011

Event: Journal Club “Amyloid-binding compounds maintain protein homeostasis during ageing and extend lifespan”

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

Alex Bishop will be presenting the paper on Friday (5/13/2011) at 4:00 PM in Roskamp Institute.

Title: “Amyloid-binding compounds maintain protein homeostasis during ageing and extend lifespan ”

Nature 472, 226–229 (14 April 2011) doi:10.1038/nature09873

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]

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

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

Title: Effect of VEGF and its receptor antagonist SU-5416, an inhibitor of angiogenesis,on processing of the beta-amyloid precursor protein in primary neuronal cells derived from brain tissue of Tg2576 mice.

Filed under: Uncategorized — Tags: , , — Gogce Crynen @ 10:32 am

Nowell (Jim) Ganey will be presenting the paper on Friday (9/17/2010) at Roskamp Institute.

Title:  Effect of VEGF and its receptor antagonist SU-5416, an inhibitor of angiogenesis,on processing of the beta-amyloid precursor protein in primary neuronal cells derived from brain tissue of Tg2576 mice.

Int J Dev Neurosci. 2010 Jul 22. [Epub ahead of print] doi:10.1016/j.ijdevneu.2010.07.231

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 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 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

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

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.

August 11, 2009

CD40L induces Abeta production via signaling by the granulocyte macrophage colony stimulating factor (GM-CSF)

Filed under: alzheimer,cd40 — Tags: , , , — admin @ 1:01 pm

Alzheimer’s disease (AD) is the most common type of dementia in the elderly. AD is mainly characterized by the accumulation of a small molecule (known as amyloid beta (Abeta)) in the brain. Many researchers have shown that the molecule CD40L is elevated in AD patients. Roskamp Institute research group headed by Dr. Michael Mullan also have recently shown that CD40L stimulation increases Abeta levels in cellular models of the disease. Furthermore, we have shown that CD40L stimulation of cells that are important for the defense of the nervous system induces increases in pro-inflammatory molecules known as cytokines. The granulocyte macrophage colony stimulating factor (GM-CSF) is one of these cytokines involved in inflammation responses in the brain. Numerous studies have correlated AD with increases in pro-inflammatory cytokines. In the cytokine paper, we have shown that CD40L stimulation increases the levels of both GM-CSF and Abetain AD cell models. We have shown that treatment of these cells with GM-CSF causes a time dependent significant increase in Abeta levels. We demonstrate that blocking GM-CSF reduces CD40L-induced Abeta production in a dose dependent manner. In addition, we show that inhibiting GM-CSF signaling by silencing the GM-CSF receptor gene significantly reduces Abeta levels to below basal levels in non-CD40L-stimulated by blocking the trafficking of Abeta’s mother protein, the amyloid precursor protein. Our results that are now published in the Journal cytokine (Volmar et al., in press) suggest that GM-CSF operates downstream of CD40/CD40L interaction and that GM-CSF modulates Abeta production.

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