Scientists at the Krembil Brain Institute have come up with a new model (AD2) for Alzheimer’s that looks at it not as a brain disease but as a chronic autoimmune disorder that attacks the brain.

Researchers from the Krembil Brain Institute have developed a novel mechanistic model (AD2) for Alzheimer’s, describing it as a chronic autoimmune disorder that targets the brain rather than a brain disease.

The findings of the study were published today in Alzheimer’s & Dementia.

Dr. Donald Weaver, co-Director of the Krembil Brain Institute and author of the paper and team “don’t think of Alzheimer’s as fundamentally a disease of the brain. We think of it as a disease of the immune system within the brain.”

More than 50 million individuals worldwide are affected by Alzheimer’s disease, the most prevalent type of dementia, with a new case being identified every three seconds. Yet there are no disease-modifying therapies to stop, prevent, or treat Alzheimer’s disease despite more than 200 clinical trials in the previous 30 years.

Dr. Weaver asserts that “We need new ways of thinking about this disease, and we need them now.” 

Up until now, most Alzheimer’s research has been based on the idea that beta-amyloid, a protein that is thought to be abnormal in the brain, clumps together. When it sticks together, it kills brain cells.

“But we believe,” the author adds, “beta-amyloid is right where it should be. It acts as an immunopeptide – a messenger within our immune system – so that, if we have head trauma, beta-amyloid repairs it. If a virus or a bacteria comes along, beta-amyloid is there to fight it.”

Dr. Weaver says that’s where the problem comes from. 

“Beta-amyloid gets confused and can’t tell the difference between a bacteria and a brain cell,” adds Dr. Weaver, “and so it inadvertently attacks our own brain cells. 

“This, then, becomes what we call an autoimmune disease. The immune system is actually attacking the host, our brain.”

In order to construct a comprehensive mechanistic model of Alzheimer’s, the study team undertook an exhaustive search that included a broad analysis of the journals and patient literatures, as well as their own studies.

The team’s findings were as follows:

• The AD2 model recognizes beta-amyloid as a physiologically oligomerizing immunopeptide and a component of a much larger and broad, highly-interconnected immunopathic process, while also attempting to harmonize other mechanistic propositions (including proteopathy, synaptotoxicity, and mitochondriopathy).

• The amino acid metabolism of L-tryptophan and L-arginine emerges as innate immune regulators within the AD2 model, alluding to new therapeutic and diagnostic modalities.

Dr. Weaver says that if we think of Alzheimer’s disease as an autoimmune disease and beta-amyloid as a normal part of our immune system, we can find new ways to come up with innovative new treatments.

“We are very excited in our lab. We think that this autoimmune theory is sound and represents a significant conceptual step forward.”

Source: 10.1002/alz.12789

Image Credit: Getty

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