NeuroTalk Support Groups - research in Alzheimer's ?

mindmystery,
if you go to PubMed and type in "drosophila alzheimer s" you should get around 60 citations. Some of them might be of interest to you as well. Some will have Free Full Text articles but some will only show abstracts of articles. A lot of this is way over my head... :)

http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed
PubMed

http://www.jneurosci.org/cgi/content/full/24/16/3899
The Journal of Neuroscience, April 21, 2004, 24(16):3899-3906; doi:10.1523/JNEUROSCI.0283-04.2004
Neurobiology of Disease
Age-Dependent Neurodegeneration and Alzheimer-Amyloid Plaque Formation in Transgenic Drosophila
Isabell Greeve, Doris Kretzschmar, Jakob-Andreas Tschäpe, Anika Beyn,Claire Brellinger, Michaela Schweizer, Roger M. Nitsch, and Rita Reifegerste

Quote:

The targeted expression of human disease genes in Drosophila has been used previously as a model system to study the complex pathophysiology and potential treatment forms of human neurodegenerative diseases such as Parkinson's disease and amyotrophic lateral sclerosis as well as polyglutamine-repeat diseases (Feany, 2000Go; Fortini and Bonini, 2000Go). Our model closely mimics main characteristics of the human AD neuropathogenesis in the eye of the fly and demonstrates that A{beta}-induced neurodegeneration is a conserved principle that acts even in flies. In particular, this system may be useful in the search of inhibitors of {beta}- or {gamma}-secretases that are currently regarded as a valid option for the treatment and prevention of AD.

http://www.med.nyu.edu/communications/news/pr_234.html
NYU School of Medicine
ALZHEIMER’S ASSOCIATION AWARDS PRESTIGIOUS GRANTS TO
THREE NATHAN KLINE INSTITUTE & NYU SCHOOL OF MEDICINE DEMENTIA RESEARCHERS
and
http://www.rfmh.org/nki/NewsEmp/content.cfm?newsid=206
Nathan Kline Institute

Quote:

Stephen D. Ginsberg, PhD, Assistant Professor of Psychiatry and Physiology and Neuroscience <snipped article>
The study hopes to identify and develop biomarkers to track the progression of dementia that can pave the way for new treatments to delay the onset of cognitive impairment and other symptoms of the disease.

Quote:

Efrat Levy, PhD, Associate Professor of Psychiatry and Pharmacology,will study a novel approach to reduce Abeta amyloidogenesis by keeping it in a soluble form that prevents its deposition. This approach builds upon Dr. Levy’s expertise in the biochemistry of the cysteine protease inhibitor cystatin C. A small sequence of cystatin C will be made so that it binds Abeta and keeps it from forming aggregates. This approach could lead to new therapies.

Quote:

Paul Mathews, PhD, Assistant Professor of Psychiatry will investigate the use of immunotherapy to reduce Abeta levels in the brain. Abeta is one of the primary problems in Alzheimer’s disease, and Dr. Mathews has developed an innovative strategy to use a vaccination approach to reduce Abeta. Using mice models, the approach will be tested and mechanisms associated with Abeta deposition and clearance will be investigated

http://molinterv.aspetjournals.org/c...t/full/5/5/292
Molecular Interventions 5:292-303, (2005)
Review
Drosophila
A "Model" Model System To Study Neurodegeneration
Alicia M. Celotto and Michael J. Palladino

http://www.nature.com/cdd/journal/v1.../4402033a.html
Cell Death and Differentiation (2007) 14, 607–615. doi:10.1038/sj.cdd.4402033; published online 25 August 2006
Abl deregulates Cdk5 kinase activity and subcellular localization in Drosophila neurodegeneration
Edited by E Baehrecke
H Lin, T-Y Lin and J-L Juang

http://www.ncbi.nlm.nih.gov/sites/en...t=AbstractPlus
Curr Opin Pharmacol. 2004 Oct;4(5):513-6.
Therapeutic targets from a Drosophila model of Alzheimer's disease.
Crowther DC, Kinghorn KJ, Page R, Lomas DA.

This is old but interesting. You may have already read it. Just put it here for interest.
http://www.nature.com/nm/journal/v8/...m0602-565.html
News and Views
Nature Medicine 8, 565 (2002) doi:10.1038/nm0602-565
Flies tangle with tau
Charlotte Schubert

Quote:

The new data help clear up the question of whether hyperphosphorylation of tau is a cause, rather than a consequence, of tangle formation. In fact the researchers saw evidence of cell death before the formation of tangles, hinting that it may be tau itself and not tangle formation per se that leads to neurodegeneration. The fly model is particularly useful for genetic screens to look for additional modifiers of tau − and this study leads the way. The authors point out that in human disease, it may be defects in modifiers of tau, rather than tau itself, that initiate the neurodegenerative process.