An experimental drug restored brain synapses in two mouse models of Alzheimer’s disease, raising hopes that it could help revive cognitive function in human dementia patients, Yale University researchers report June 1 in the journal Science Translational Medicine.
While much research in Alzheimer’s has centered on reducing levels of beta-amyloid plaque in the brain that is a hallmark of the disease, recent studies have suggested that immune system response in the brain also plays a role in memory loss in patients.
Some scientists now believe that cognitive decline in Alzheimer’s patients results from a loss of synaptic connections between neurons caused by a steady accumulation of beta-amyloid protein in the brain which in turn unleashes a chronic immune system response to the intruder. The end stages of the disease lead to the death of neurons.
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