Age, Biography and Wiki

Robert Moir (Robert David Moir) was born on 2 April, 1961 in Kojonup, Australia, is a medical researcher. Discover Robert Moir's Biography, Age, Height, Physical Stats, Dating/Affairs, Family and career updates. Learn How rich is He in this year and how He spends money? Also learn how He earned most of networth at the age of 58 years old?

Popular As Robert David Moir
Occupation N/A
Age 58 years old
Zodiac Sign Aries
Born 2 April 1961
Birthday 2 April
Birthplace Kojonup, West Australia, Australia
Date of death December 20, 2019
Died Place Milton, Massachusetts, US
Nationality Australia

We recommend you to check the complete list of Famous People born on 2 April. He is a member of famous Researcher with the age 58 years old group.

Robert Moir Height, Weight & Measurements

At 58 years old, Robert Moir height not available right now. We will update Robert Moir's Height, weight, Body Measurements, Eye Color, Hair Color, Shoe & Dress size soon as possible.

Physical Status
Height Not Available
Weight Not Available
Body Measurements Not Available
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Who Is Robert Moir's Wife?

His wife is Julie Alperen Elena Vaillancourt

Family
Parents Not Available
Wife Julie Alperen Elena Vaillancourt
Sibling Not Available
Children 3

Robert Moir Net Worth

His net worth has been growing significantly in 2022-2023. So, how much is Robert Moir worth at the age of 58 years old? Robert Moir’s income source is mostly from being a successful Researcher. He is from Australia. We have estimated Robert Moir's net worth , money, salary, income, and assets.

Net Worth in 2023 $1 Million - $5 Million
Salary in 2023 Under Review
Net Worth in 2022 Pending
Salary in 2022 Under Review
House Not Available
Cars Not Available
Source of Income Researcher

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Timeline

2018

Attempting another request for a grant from the NIH in 2018 for further research into the herpes virus and Alzheimer's was rejected before money was found in early 2019.

2016

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 lack of being a full professor and poor previous funding. He would later be funded by CureAlz and again attempted to publish in 2017 before finally being published in 2018.

2010

In 2010 funding was given to fund himself, a doctoral student and $400 worth of mice. Testing proved the theory in live Alzheimer's mice and he then attempted to publish in six journals in 2014 but was rejected by peers. The paper would eventually be published in 2016 by the journal Science Translational Medicine. When the research article was published in 2016, it was regarded as one of the top five advances in Neurology for that year.

2007

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. Tanzi's work at the time focused on genes that increased the risk of getting Alzheimer’s disease and the inbuilt ability of some to fight germs so Moir proposed that beta-amyloid might have an anti-microbial effect in Alzheimer's. The theory was that the beta-amyloid creates a plaque that captures the dangerous microbes and protects the brain but too much build-up of the plaque could become toxic and cause Alzheimer’s disease to develop. Tanzi encouraged Moir to continue research into the use of beta-amyloids to kill pathogens, funding it out of the former's research funding. He succeeded in this theory 2009 when he finally replicated the process in laboratory petrie dishes. The next step was to try the theory in Alzheimer and healthy brain tissue with good results and attempted to publish the results in Science and three other journals and was rejected but finally succeeded in 2010.

2006

Moir struggled for many years to obtain funding for his research, like many in his field, as those reviewing funding applications and those vetting papers for possible publication, viewed alternative explanations for the cause of Alzheimer's Disease as wrong. 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. In 2010 further funding from NIH/National Institute of Allergy and Infectious Diseases (NIAID) for the study of the Abeta protein of Alzheimer's Disease is an antimicrobial peptide and in 2019, again from the NIH/NIA for research into the Antimicrobial activities of Abeta in Alzheimer's disease brain.

2004

Moir was married twice. First to Elena Vaillancourt from whom he divorced in 2004, and secondly to Julie Alperen.

1996

On completion of high school, he studied biochemistry at the University of Western Australia with one of his microbiology lecturers being Nobel Prize winner Dr Barry Marshall, who discovered that H. pylori cause ulcers. He received his PHD in 1996 from the University of Melbourne, supervised by neuropathologist Dr Colin Masters.

1994

Moir immigrated to the United States in 1994 to work in Dr Rudolph Tanzi's laboratory at Harvard University as an Alzheimer’s biochemist. He had met Tanzi at a medical conference in Amsterdam. Moir was also able to purify and produce quantities of the molecule which the brain used to make the beta-amyloid. He concentrated initially in Tanzi's work on establishing what genes affected the risk of Alzheimer’s disease. He continued working for Tanzi as a post-doctoral fellow and would eventually become an assistant professor in neurology at Harvard Medical School and the Massachusetts General Hospital and his own laboratory at the institution.

1961

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.