What if the bad-boy protein of Alzheimer’s disease – amyloid beta – isn’t so bad after all?
Harvard researchers found themselves asking that question several years ago after noticing remarkable similarities between amyloid beta, thought to be a major player in the disease’s progression, and proteins active in the body’s immune system.
That discovery has blossomed into a new avenue of investigation against the nation’s leading cause of dementia, sixth-deadliest illness, and – according to a 2011 survey – the runner-up to cancer in health fears among the public.
Led by Robert Moir, an assistant professor in neurology at Harvard Medical School (HMS) and Massachusetts General Hospital (MGH), and Rudolph Tanzi, Joseph P. and Rose F. Kennedy Professor of Child Neurology and Mental Retardation at HMS and MGH, the work is focused on whether the development of amyloid beta plaques in the brain – a hallmark of Alzheimer’s disease and the target of several recent drug candidates – might in many cases be a response to infection.
Proven correct, the explanation would fill a significant blank in our framework for the causes of Alzheimer’s disease, create a new understanding of amyloid beta’s role in the body, and possibly open new fronts for treating or preventing the condition by attacking infection before plaques begin to form.