Posts by Robert Moir, PhD
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The Innate Immune Protection Hypothesis of Alzheimer's Disease
Alzheimer's disease research at Massachusetts General Hospital has led to a new immune protection hypothesis that may lead to new treatment and prevention options.
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Infectious Disease May Play a Role in Alzheimer’s disease
Robert Moir, PhD, a neurobiologist at Massachusetts General Hospital, shares groundbreaking new research suggesting amyloid is actually an immune response that works to trap and neutralize invading pathogens. This discovery suggests infection may play a role in Alzheimer’s disease and is helping point the way towards urgently needed new treatment strategies.
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Unconventionality in Alzheimer's Research and the Pursuit of Validation
From the 1980s, scientists understood beta-amyloid were a toxic byproduct that, when deposited in the brain, caused Alzheimer's. However, Dr. Robert Moir followed an unconventional research path, and revealed that the development of amyloid plaques might be an immune response to microbe infections.
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Brain Infection with Herpes Virus May Accelerate Progression of Alzheimer's Disease
Laboratory studies at Mass General suggest that active herpes infections in the brain may accelerate amyloid deposition and the progression of Alzheimer's disease.
Biography
Robert Moir’s research focuses on the biochemical and cellular mechanisms of neurodegeneration in Alzheimer's disease (AD) and aging. His work has uncovered new therapeutic targets aimed at preventing the accumulation of beta-amyloid (Aß), the primary neurotoxic agent in AD. Moir was the first to identify the low-density lipoprotein receptor protein (LRP) as the mediator of an important early step in Aß production in the brain. Today, LRP-mediated Aß clearance pathways are increasingly recognized as major targets for therapeutic intervention. His work revealed the importance of metals in the pathological aggregation of Aß, leading directly to the investigation of the copper and zinc chelator clioquinol in clinical trials for AD. Moir has also helped establish Aß’s role in the formation of eye lens cataracts in AD patients, which could lead to better diagnosis of the disease. His studies on the immune response to amyloid have revealed potential abnormalities in protective Aß-reactive autoantibodies in AD patients. Moir’s most recent studies have identified the normal biological function of Aß. He found that Aß serves as a natural antibiotic, acting as part of the innate immune system to trap and kill pathogens invading the brain. This novel discovery suggests AD may be an inappropriate response to a real or falsely perceived infection in the brain. This finding may also shed light on the pathological mechanisms associated with other major amyloid-associated diseases, including diabetes and arteriosclerosis.
Dr. Moir received his PhD in neurobiology in 1996 from the University of Melbourne in Australia, where he worked under the mentorship of Prof Colin Masters, one of the founders of the modern field of Alzheimer's disease (AD) research. In 1994, Moir moved to MGH for postdoctoral training in the Genetics and Aging Research Unit with Dr. Rudolph Tanzi. He was appointed an Assistant Professor of Neurology at HMS and MGH in 2006.
