THURSDAY, May 3 (HealthDay News) -- Reducing the amount of tau protein in a mouse model of Alzheimer disease prevents cognitive deficits and protects neurons from damage due to overexcitation, according to study findings published in the May 4 issue of Science.
Erik D. Roberson, M.D., of the Gladstone Institute of Neurological Disease, University of California San Francisco, and colleagues generated mice that produced human amyloid precursor protein, the precursor of amyloid-beta peptide, and lacked one or both copies of the tau protein gene.
The reduction in tau protein prevented deficits in learning and memory, and prevented early death with no effect on plaque load or the level of amyloid-beta peptide. Tau reduction also did not prevent neuritic dystrophy or the aberrant sprouting of hippocampal axons. However, neurons in mice lacking at least one copy of the tau gene were protected from damage due to aberrant overexcitation. Tau reduction had no adverse effect on health or cognition in the mice, the authors note.
"Thus, tau reduction can block amyloid-beta- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer disease and related conditions," Roberson and colleagues conclude.
Abstract
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