Clearance of beta amyloid accumulation within neurons stops memory decline in mice
Researchers at UC Irvine have identified a trigger at the molecular level that marks the onset of memory decline in mice genetically engineered to develop brain lesions – in the form of plaques and tangles – associated with Alzheimers disease. The trigger is a protein called "beta amyloid" that accumulates within neurons in the mices brains. Although several researchers have studied the association between beta amyloid and memory, the UCI research team is the first to identify that early beta amyloid accumulation within neurons is the trigger for the onset of memory decline in Alzheimers.
"This finding has important and useful implications for the pharmaceutical industry in terms of developing drugs that can target beta amyloid as soon as it accumulates within the neurons," said Frank LaFerla, principal investigator of the research project, associate professor of neurobiology and behavior, and co-director of the UCI Institute for Brain Aging and Dementia. "Once the plaques and tangles form, it is too late."
Iqbal Pittalwala | EurekAlert!
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