A Scientist’s 10-year Odyssey to Find Funding for Important, Out-of-the-Box Research

Posted December 13, 2018

Cure Alzheimer’s Fund has, as a founding principle, a commitment to funding innovative research ideas that may not meet the criteria for funding from the National Institute of Health. Curing Alzheimer’s disease will require audacious ideas that tackle disease mechanisms by leaving no stone unturned. A recent article in STAT tells the story of the 10-year odyssey that Dr. Rob Moir of Massachusetts General Hospital encountered while trying to find funding for an unconventional theory. The story highlights how he ultimately received a $500,000 grant from Cure Alzheimer’s Fund to pursue his hypothesis. His hunch that inflammation played a more critical role in synapse loss and cell death during Alzheimer’s disease than beta-amyloid accumulation was validated through this research.

www.statnews.com/2018/10/29/alzheimers-research-outsider-bucked-prevailing-theory/

Dr. Moir and his team of scientists asked an intriguing question: how does the presence of a virus like herpes influence the spread of amyloid beta? To test this hypothesis, the scientists used a 3D model for Alzheimer’s disease referred to as Alzheimer’s-in-a-dish in order to investigate the effect of the herpes virus in the brain.

The infection model for Alzheimer’s disease has been around as long as 1907 when Alois Alzheimer (who first described the disease) proposed infection as a possible underlying cause. Only recently has this hypothesis received increased attention from those researching the disease – in large part due to influential work from Dr. Moir and his laboratory.

Experiments from Moir’s lab have provided experimental evidence for a non-traditional role for amyloid beta. Specifically, amyloid beta protects against infection from the herpes virus as particles from the invading virus are trapped and inactivated by amyloid plaques. Moir’s work was published in Neuron where he concluded that amyloid beta traps the herpes virus in deposits called amyloid. High amyloid accumulation is a criterion for diagnosis with Alzheimer’s disease.

This study suggests that while active herpes infections may drive amyloid deposition and the progression of Alzheimer’s disease, amyloid beta may be playing a previously underappreciated role in providing a protective immune response to infection.

The Research Papers are available in Neuron:

Alzheimer’s Disease-Associated B-Amyloid Is Rapidly Seeded by Herpesviridae to Protect Against Brain Infection

Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of molecular, Genetic, and Clinical Networks by Human Herpes Virus

Dr. Moir’s research has also been highlighted on NPR. To learn more about the link between Alzheimer’s disease and the immune system as well as his collaborations with Dr. Rudy Tanzi, follow this link.

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