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

A Decreasing Ability to Learn Among Aging Healthy Carriers of APOE 4
Nunzio Pomara, M.D., Professor in the Department of Psychiatry, NYU Langone Medical Center; Director of the Geriatric Psychiatry Program, Nathan S. Kline Institute
EMBARGOED FOR RELEASE WEDNESDAY, July 30, 2008, at 1 PM CT

A new study by NYU researchers at the Nathan Kline Institute suggests that a major genetic risk factor for Alzheimer's disease, apoE 4, may exert its adverse effects long before clinical symptoms of the disease emerge. During this critical period they believe there may be a gradually decreasing ability to learn new material, and subsequently form new memories. The scientists evaluated 184 healthy adults, ages 38 to 80 (64 people carried the apoE4 allele), using standardized measures of verbal learning and memory, such as learning a list of words. At younger ages, surprisingly, those with the apoE 4 genetic risk factor significantly outperformed those without it. By ages 60 to 64 and older, however, performance in the apoE 4 group dropped below the non-apoE 4 group.
Presentation # HT-3577

Genetic Mutation Linked to a More Abundant Form of Alzheimer's Protein
Allal Boutajangout, PhD, Research Assistant Professor, Department of Medicine and Psychiatry at NYU Langone Medical Center
EMBARGOED FOR RELEASE UNTIL WEDNESDAY July 30, 2008 at 4:00 p.m. CT

NYU researchers found that a specific gene mutation previously associated with an increase in production of an Alzheimer's disease-causing protein, amyloid beta, also promotes the entanglement of another protein, tau, which also is associated with the neurodegenerative disease. Mice that produced human types of tau while expressing the gene mutation showed a significant increase in the harmful form of the tau protein in the brain. The research provides a new model for Alzheimer's onset and progression.
Presentation #04-01-05

Study Further Ties Digestion of Harmful Protein to Alzheimer's Disease
Dun-Sheng Yang, 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 27, 2008 at 12:30 p.m. CT

NYU researchers genetically enhanced the activity of digestive enzymes in the nerve cells of mice that were susceptible to producing an overabundant amount of amyloid beta, the abnormal protein found in the plaques littering the brains of people with Alzheimer's. The mice showed lower amounts of the protein in parts of the brain responsible for advanced thinking, learning and memory—evidence that their brain cells were more efficient at digesting and expelling the toxic, misfolded protein, the researchers report. The study shows that the failure to degrade amyloid beta in lysosomes containing the digestive enzymes is an important factor in Alzheimer's disease. Amyloid beta and another protein called tau are associated with the disease, but it hasn't yet been proven definitively that either actually causes the disease.
Presentation # P1-059