Mar. 23 --
WEDNESDAY, June 6 (HealthDay News) -- Stroke and head injury trigger a cellular chain of events that increases the risk of Alzheimer's disease, a new study says.
Learning more about this process could help in the development of treatments to protect against Alzheimer's disease.
Researchers at the MassGeneral Institute for Neurodegenerative Disorders identified how the death of brain cells caused by stroke or head injury may boost levels of amyloid-beta protein. Alzheimer's is characterized by the presence of amyloid-beta plaques in the brain.
"We have discovered how a stroke can trigger a series of biochemical events that increase amyloid-beta production in the brain. These findings raise the prospect of novel therapies that could interfere with this process and reduce the risk of Alzheimer's disease in stroke or head trauma patients," study author Dr. Giuseppina Tesco, of the genetics and aging research unit, said in a prepared statement.
It was already known that stroke and head injury could increase a person's risk of developing Alzheimer's, but the mechanism behind that increased risk wasn't known.
The authors of this study conducted a series of experiments and found that damaged brain cells undergo apoptosis (cell death) and release a compound called caspace, which breaks down a protein called GGA3.
GGA3 helps control levels of an enzyme called beta-secretase (BACE), which contributes to the formation of beta-amyloid. A lack of GGA3 results in increased levels of BACE which, in turn, leads to increased beta-amyloid production.
The researchers also noted that beta-amyloid itself is toxic to brain cells and may cause further death of brain cells. That may lead to a cycle of continued brain cell death and beta-amyloid production.
The study is published in the June 7 issue of Neuron.
The U.S. National Institute of Neurological Disorders and Stroke has more about Alzheimer's disease.
SOURCE: Massachusetts General Hospital, news release, June 6, 2007