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Study outlines how stroke, head injury can increase risk of Alzheimer's disease

including a stroke, can lead to the production of amyloid-beta. Damaged brain cells undergo apoptosis, releasing caspase which also breaks down GGA3. Without enough GGA3 to help transport BACE to lysosomes, levels of BACE rise and lead to increased amyloid-beta production. Amyloid-beta itself is toxic to brain cells, so it may cause further apoptosis, leading to a vicious cycle of continued cell death and amyloid-beta production.

The importance of GGA3s control of BACE levels was supported by the observation that, in brain tissue from Alzheimers patients, reductions in GGA3 corresponded with elevations in BACE, particularly in those areas most affected by the disease.

Our findings also shed new light on how the aged brain becomes more vulnerable to AD, since any insult to the brain head injury, stroke, or the mini-strokes called TIAs can set off this process and turn up BACE activity, says Rudolph Tanzi, PhD, director of the Genetics and Aging Research Unit and senior author of the Neuron paper. Therapies that protect GGA3 from caspase cleaving might be able to reduce the risk of AD or the more transient type of dementia that can occur after such injuries. Tanzi is a professor of Neurology at Harvard Medical School, where Tesco is an assistant professor.


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Contact: Sue McGreevey
smcgreevey@partners.org
617-724-2764
Massachusetts General Hospital
6-Jun-2007


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