Robert Moir

Robert David Moir (2 April 1961 – 20 December 2019) was an Australian-born medical research scientist who theorized that the over-accumulation of beta-amyloid, which had formed to protect the brain against microbes, aided the development of Alzheimer's disease in the human brain.

Early life He was born in Kojonup in Western Australia to Terrence and Mary Moir who were farmers and had three siblings, Margaret, Andrew and Catherine. He said he only learnt to read and write at age twelve but became an avid reader of all things scientific.

Career Moir immigrated to the United States in 1994 to work in Rudolph Tanzi's laboratory at Harvard University as an Alzheimer's biochemist.

In 2007 he came across a research article about an antimicrobial peptide called LL37 that killed viruses, fungi and bacteria in the brain and which he thought could be a twin of the beta-amyloid, another antimicrobial.

In 2010 funding was given to fund himself, a doctoral student and $400 worth of mice.

In 2016, he attempted to gain funding from the National Institutes of Health (NIH) to research whether herpes simplex virus 1 (HSV-1), which causes cold sores and can reach the brain, that might promote both amyloid plaques and tau tangles but was rejected when the third funding reviewer criticized the proposed research as being a possible minor cause of Alzheimer's, Moir's status as less than a full professor, and his poor prior funding. In 2006 he received funding from the NIH/National Institute on Aging (NIA) for targeting cross-linked amyloid protein species as a therapy for Alzheimer's Disease. The Moir Lab focused on the biochemical and cellular mechanisms involved in neurodegeneration in Alzheimer's disease and ageing.