Find all causes of Alzheimer's disease and a cure

Some individuals develop significant levels of amyloid beta plaques and tau tangles in their brains but never show clinical symptoms of dementia. The leading hypothesis to explain these resilient brains is that their neuroimmune system responds to Alzheimer’s-related pathology with lower levels of neuroinflammation, which is common in symptomatic cases of the disease. However, the factors triggering excessive neuroinflammation remain unclear.

Neuroinflammation is a healthy response to debris and pathology in the brain, but this response must be appropriate in level and duration or it can become damaging rather than protective. The pathology that leads to Alzheimer’s disease starts to develop many years before symptoms appear. Amyloid beta accumulates in the brain as plaque bundles, followed by the formation of tau tangles. Synapses are the points of communication between neurons and are essential for memory and cognition. Severe loss of synapses and neurons — neurodegeneration — thus disrupts the circuitry that encodes thought and memory. The neuroinflammatory response to Alzheimer’s-related pathologies is a more direct driver of the loss of neurons and their synapses than are the pathologies themselves. Understanding how the neuroimmune response in resilient people differs from that of people who develop clinical Alzheimer’s disease could allow the development of therapies designed to replicate this resilience in all people.

Find out more: https://bit.ly/49IeqfN

Teresa Gomez-Isla, M.D., Massachusetts General Hospital/ Harvard Medical School

Karen E. Duff, Ph.D., University College London, England