Close up of a man holding his head on black.

A new research model suggests that Alzheimer’s disease may be a result of autoimmune disease in the brain, rather than a disease of the brain as many have previously thought.

Donald F. Weaver of Krembil Research Institute at the University of Toronto, the study’s author, conducted a systematic review of journal and patent literatures, using a variety of search algorithms, to create “an innovative broadly encompassing model of Alzheimer’s disease (AD) that harmonizes multiple divergent theories into a unified comprehensive explanation.”

“The findings led to an integrated new molecular model for AD: ‘Alzheimer’s disease as an autoimmune disease’ (“AD2”),” Weaver wrote in the study. “In AD2, AD is a brain-centric disorder of innate immunity involving concurrent autoimmune and autoinflammatory mechanisms.”

The research specifically studies the role that amyloid beta protein plays in Alzheimer’s disease. Amyloid beta (Aβ) is released in the brain as an autoimmune or antimicrobial response to a specific pathogen or damage associated event, such as an infection, trauma, stroke or pollution.

However, the study theorizes that Aβ’s antimicrobial properties may result in a misdirected attack upon “self” neurons in the brain, arising from the electrophysiological similarities between neurons and bacteria. This can result in the further release of Aβ, leading to a chronic, self-perpetuating cycle of breakdown of the brain’s neurons.

The study found Alzheimer’s disease is a multi-factorial complex disorder that likely requires a combination of existing drugs and new therapeutic treatments, which must include agents directly targeting the innate autoimmunity that is crucial to Alzheimer’s disease progression.

“Indeed, as has been suggested for other neurological disorders, there may be a need to devise selectively non-selective drugs (“dirty drugs” acting as a magic shotgun rather than a magic bullet) that therapeutically interact with several complementary molecular targets,” Weaver wrote in the study.

Operating grants from the Canadian Institutes of Health Research, the Weston Foundation, the Krembil Foundation and a Harrington Scholar-Innovator Award from the Harrington Discovery Institute funded the research. The article appeared in the Sept. 27 issue of Alzheimer’s & Dementia, the Journal of the Alzheimer’s Association.