Prominent neurologist awarded grant to research Alzheimer’s as an autoimmune disease
Alzheimer’s is the most common cause of dementia; according to the Alzheimer’s Association, Alzheimer’s disease accounts for up to 80% of dementia cases.
Although little is still known about this disease, which causes significant loss of memory and other cognitive abilities, the most well-accepted hypothesis is that Alzheimer’s is caused by the build up of a protein called beta amyloid. When too much beta amyloid is accumulated in the brain, toxic clumps of the protein, called plaques, can form. These plaques are believed to be the culprit for Alzheimer’s; as a result, recent clinical trials have aimed to find a way to target and reduce the amount of plaques in the brain.
However, a prominent neurologist and medical researcher from Toronto, Ontario, Canada has put forth a new hypothesis on the development of Alzheimer’s. Dr. Donald Weaver theorizes that beta amyloid is actually a normal part of the brain’s innate immune system, and is there to kill bacteria and serve as a messenger protein. When the body’s immune response is triggered by an infection, trauma, or exposure to noxious substances, brain cells are triggered to release beta amyloid.
The problem arises, however, when beta amyloid mistakes brain cells for bacteria, and begins to kill these cells instead. This leads to fragments being created in the brain, which go on to trigger the continued release of beta amyloid. The result is a self-perpetuating cycle of releasing beta amyloid and killing more brain cells, resulting in a chronic disease.
Dr. Weaver’s theory on Alzheimer’s as an an autoimmune disease has garnered the attention of the medical community. He has been awarded the silver Oskar Fischer Prize, a grant worth US$400,000 from the University of Texas at San Antonio, to pursue research related to his theory.
Dr. Weaver believes that by exploiting the body’s natural way of controlling the immune system, Alzheimer’s symptoms can be reduced, and the disease could even be prevented. He commented, “If we accept the fact that Alzheimer’s disease is an immune-based disease that has certain triggers, then I think that we need to go back and revisit the risk factors.” Examples of risk factors include air pollution, head trauma, and genetic susceptibility.
Ultimately, Dr. Weaver’s research represents hope for a new way of tackling Alzheimer’s disease. Even more exciting is that Dr. Weaver’s research may have applicability beyond Alzheimer’s to other neurological conditions as well, such as Parkinson’s, Multiple Sclerosis (MS), and Encephalitis.
Jenny Hsieh, director of the University of Texas at San Antonio’s Brain Consortium, believes it’s important to provide researchers the opportunity to pursue ideas that are outside the box. “We just need people to be able to work on different ideas…because the bottom line is all of the current approaches to Alzheimer’s disease [are] not working.”
To learn more about Dr. Weaver and his work, visit: www.weaverlab.ca