The beta-amyloid hypothesis has dominated Alzheimer’s disease research for nearly 35 years. It proposes that plaques, comprised of the protein beta-amyloid, destroy synapses and stimulate the development of neurofibrillary tangles of the tau protein, which kills neurons in patients with the disease. Resultantly, neuroinflammation is triggered, which destroys more neurons and ultimately leads to dementia.
Thus far, the management of amyloid plaques in symptomatic patients has been the primary focus of interventions. However, to date, the treatments derived from this hypothesis have had no significant impact on the disease.
Research led by Rudolph E. Tanzi, PhD, co-director of the McCance Center for Brain Health and vice-chair of the Department of Neurology at Massachusetts General Hospital, and the late Robert D. Moir, PhD, argues that beta-amyloid may actually be part of a necessary neuroprotective system, first reported in 2010 in Plos One, and further described in Neuron.
If validated, their idea, called the innate immune protection hypothesis, would require a fundamental reappraisal of Alzheimer’s disease etiology and treatment strategies.
The hypothesis is that the antimicrobial activities of Alzheimer’s disease hallmarks, beta-amyloid plaques and tau tangles, evolved into neuroprotective responses guarding against brain infection that then leads to neurotoxic consequences
