UCLA scientists pinpoint a possible physical origin of Alzheimer's disease
Discovery suggests new ways to treat disorder's cause, not just symptoms
For some time, scientists have blamed Alzheimer's disease on a small molecule called amyloid beta protein (A beta) that leaves large gummy deposits in the brain. Recent studies suggest that these A beta proteins stick together to form floating toxic clumps that kill brain cells. Now, UCLA scientists have identified a tiny loop in A beta as the likely culprit behind the adhesion process.
The UCLA team discovered that gene mutations in A beta increase the loop's flexibility, enabling it to join easily with loops from other A beta proteins and form clumps. The loop also appears in the region of the protein that regulates how â€” and how much â€” A beta is made.
Current drugs treat the symptoms of Alzheimer's but not the disease's underlying cause. By shedding light on how toxic A beta formations arise in the brain, the UCLA discovery could aid the design of new drugs that both block the production of A beta and prevent it from clumping.
Principal investigator David Teplow, professor of neurology at the David Geffen School of Medicine at UCLA, is available for interviews.
The National Institute of Neurological Disorders and Stroke, the National Institute on Aging and the Alzheimer's Association supported the study.
The Proceedings of the National Academy of Sciences published the findings in its Oct. 10 online early edition. For a PDF of the study, see www.eurekalert.org/pio/tipsheetdoc.php/237/zpq7481.pdf.
Alzheimer's disease afflicts some 5 million Americans and an estimated 24 million people worldwide. Half of people over 85 may suffer from the fatal disorder, which slowly robs individuals of their memory and ability to think and function independently.