NYU Langone Medical Center's tip sheet to the International Conference on Alzheimer's Disease 2008

Study Suggests a Link Between Amyloid and Memory
Paul M. Mathews, PhD, Assistant Professor, Department of Psychiatry, NYU Langone Medical Center; Research Scientist, Center for Dementia Research, Nathan S. Kline Institute
EMBARGOED FOR RELEASE UNTIL SUNDAY, JULY 28, 2008 at 3:00 p.m. CT

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

Early Phases of Creating a Vaccine against Prion Disease
Thomas Wisniewski, MD, Department of Pathology at NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL TUESDAY, July 29, 2008 at 11:30 a.m. CT

In an animal study, NYU researchers bolstered immunity against a toxic and infectious version of the prion protein, which causes a group of brain diseases, including mad cow's disease. By injecting a safe, reconfigured form of the protein into the body cavity of mice, in addition to orally delivering a neutral bacterial booster, animals could produce more antibodies against the prion protein in the mouth and blood system, preventing access of the infectious prions to the brain. The inoculated mice remained symptom free for 400 days after exposure to infectious prion, while their brains were free from the disease causing protein. The finding has the potential to safely curb prion diseases, such as chronic wasting disease and variant Creutzfeld-Jacob disease, which are thought to be spread by oral exposure to prion.
Presentation # S3-01-04