Alzheimer’s Project Focuses on Role of Brain Inflammation
August 20, 2007
Scientists at the University of Rochester Medical Center have received $1.37 million to continue their work looking at some of the earliest events that occur at the start of Alzheimer’s disease – a condition that now generally goes undetected until the death of key brain cells has been underway for decades.
The team led by William Bowers, Ph.D., assistant professor of Neurology and a scientist in the Center for Aging and Development Biology, is focusing on the role of inflammation in the evolution of the disease. Just as rheumatoid arthritis can ravage the body’s joints because of the inflammation it causes, scientists are realizing that the same thing happens to the brain in patients with Alzheimer’s disease. The brain can be under assault for decades as the body attempts to fend off some perceived threat.
“The inflammatory response in the brain of a person with Alzheimer’s appears to happen very slowly,” said Bowers. “It may be that initially, the body is responding to some type of insult or problem. But as the body tries to correct that problem with recurring cycles of inflammation, the process snowballs and goes beyond the point of no return – inflammation begins damaging the brain, and the death of brain cells is the eventual outcome.”
Exactly why the inflammatory process begins remains a major question for researchers. Some people may be genetically susceptible to such a process. Other possibilities include a viral infection, a head injury, or the gradual buildup of a toxic protein known as amyloid-beta.
Bowers’ group is focusing on the role of a chemical messenger known as TNF (tumor necrosis factor) that some brain cells emit. TNF is a major player in inflammation, and scientists know that its level is higher in certain brain regions in people with the disease. Bowers’ team has shown that the same is true in mice especially prone to developing signs of Alzheimer’s disease, including accumulations of amyloid-beta in the brain and distinctive tangles within neurons. But exactly how TNF may be contributing to the disease is unknown.
Drugs that target TNF are now used in people to treat diseases like rheumatoid arthritis, and scientists are beginning to explore the use of such medications in patients with Alzheimer’s disease. Bowers’ studies are crucial to understanding how such medications might work, and to perhaps creating new drugs to reduce the inflammation.
The new funding, from the National Institute on Aging, enables Bowers and his team to continue the research for five more years. Bowers also has funding from NIA to try to create a vaccine that would customize the body’s immune response to amyloid-beta, a key contributor to Alzheimer’s.