By manipulating levels of the beta amyloid peptide, which accumulates in brain plaques in people with Alzheimer's disease, NYU researchers have found that the peptide not only plays a toxic role in the neurodegenerative disease but also is crucial in modulating learning and memory consolidation in the normal brain. The rat study, which controlled peptide levels in a region of the brain that is important in learning and memory, suggests that its disruption may be one of the underlying causes of nerve dysfunction during Alzheimer's disease pathogenesis.
Presentation #02-02-01
Dysfunctional Transporters in Nerves Related to Alzheimer's
Seonil Kim, Ph.D student, Sackler Institute for Graduate Biomedical Sciences, NYU Langone Medical Center, Graduate Training Program in Cellular and Molecular Biology, Nathan S. Kline Institute and Ralph Nixon, M.D., Ph.D., Professor of Psychiatry and Cell Biology, NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL TUESDAY, JULY 29, 2008 at 12:30 p.m. CT
An NYU study found that membrane vesicles that are essential for the trafficking of materials across nerve cells are an important factor in the pathology of Alzheimer's disease. Mouse neurons which over-produce a precursor to the amyloid protein closely linked to Alzheimer's disease development were unable to shuttle the vesicles to their proper destinations in nerve cells, causing them instead to enlarge abnormally and accumulate. The impeded transport of these vesicles, according to the researchers, may affect communications within and between nerve cells that are critical for cognition and when disrupted can lead to the neurodegeneration of Alzheimer's disease.
Presentation # PS-410
| Contact: Bob Brody bobbrody@hotmail.com 212-404-3555 NYU Langone Medical Center / New York University School of Medicine Source:Eurekalert |