The Krembil Brain Institute of the University Health Network has proposed a new mechanistic model (AD2) for Alzheimer’s disease as an autoimmune disease, which sees it not as a brain disease but as a chronic autoimmune condition that attacks the brain.
Today, this groundbreaking research was published in Alzheimer’s & Dementia.
“We do not view Alzheimer’s as a fundamentally brain disease. Dr. Donald Weaver, co-director of the Krembil Brain Institute and co-author of the study, describes the condition as a disease of the brain’s immune system.
Alzheimer’s disease, the most prevalent form of dementia, affects over 50 million people worldwide, with a new case diagnosed every three seconds. Even though more than 200 clinical trials have been done over the past 30 years, there are still no drugs that can stop, slow down, or treat Alzheimer’s.
Dr. Weaver states, “We need new ways of thinking about this disease immediately.” To date, the majority of Alzheimer’s research approaches have been based on the theory that an abnormal protein called beta-amyloid aggregates in the brain. And when it aggregates, it destroys brain cells. ”
However, we believe beta-amyloid levels are appropriate. It functions as an immunopeptide—a messenger within our immune system—so that beta-amyloid can repair head trauma. If a virus or bacteria appears, beta-amyloid will be there to combat it. ”
Therein lies the problem, according to Dr. Weaver. “Beta-amyloid is confused and cannot distinguish between a bacterium and a brain cell; therefore, it attacks our own brain cells.” This becomes what we refer to as an autoimmune disease. In actuality, the immune system is attacking the host, our brain.
According to the team’s findings,
- In order to develop a comprehensive mechanistic model of Alzheimer’s, the research team conducted a thorough search, including a wide-ranging review of journal and patient literature as well as their own studies.
- The AD2 model seeks to harmonize other mechanistic hypotheses (such as proteopathy, synaptotoxicity, and mitochondriopathy) while recognizing beta-amyloid as a physiologically oligomerizing immunopeptide and a component of a much larger, broader, and highly interconnected immunopathic process.
- The L-tryptophan and L-arginine amino acid metabolisms emerge as regulators of innate immunity in the AD2 model, pointing to new diagnostic and therapeutic approaches.
Dr. Weaver says that rethinking Alzheimer’s disease as an autoimmune disease and beta-amyloid as a normal part of our immune system makes it easier to come up with new treatments.
“We are very ecstatic in the laboratory. We consider this autoimmunity theory to be sound and a significant conceptual advance.
