Bruce Yankner, MD, PhD
|Hospital Title||Senior Associate in Medicine|
|Academic Title||Professor of Neurology|
300 Longwood Avenue
Boston MA 02115
Bruce Yankner's research focuses on neurodegenerative mechanisms in Alzheimer's disease and Down's syndrome. His laboratory has provided evidence that the beta amyloid protein causes neuronal cell death, which may contribute to the pathogenesis of dementia in Alzheimer's disease. He and his colleagues are currently focusing on the function of the presenilin genes, which cause familial Alzheimer's disease, and on environmental factors that may contribute to Alzheimer's disease.
Recently, his team demonstrated--in samples of tissue from older brains--that activity slows in genes involved in learning and memory but increases in genes linked to DNA repair. Yankner postulates that the surge in repair-gene activity is the brain's way of trying to compensate for the damage. The researchers also found the greatest variability in gene activity from person to person in tissue from the 40-to-70 age group. A goal of future research will be to understand the resons for variation among individuals.
Yankner's group has also been able to prevent gene damage in nerve cells by engineering them to make more gene-repair proteins. The researchers are working toward preventing the same damage in the living brain.
About Bruce Yankner
Bruce Yankner received both his MD and a PhD in Neurobiology from Stanford University School of Medicine. He completed an internship at Stanford University Hospital and residency in neurology at Massachusetts General Hospital in Boston.
In 2003 he received MetLife Foundation's Award for Medical Research in Alzheimer's Disease.
Lu T, Pan Y, Kao SY, Li C, Kohane I, Chan J, Yankner BA. Gene regulation and DNA damage in the ageing human brain. Nature 2004; 429: 883-891.
Ebinu JO, Yankner BA. A RIP tide in neuronal signal transduction. Neuron 2002; 34: 499-502.
- Busciglio J, Pelsman A, Wong C, Pigino G, Yuan M, Mori H, Yankner BA. Altered metabolism of amyloid beta precursor protein is associated with mitochondrial dysfunction in Down's syndrome. Neuron 2001; 33: 677-688.