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.