Researchers examined mouse models and human tissue and found that beta-amyloid bonded with the norepinephrine receptor, resulting in GSK3-beta enzyme activation and tau toxicity, but the norepinephrine receptor-blocking idazoxan treatment prompted enzyme deactivation and curbed tau toxicity in mice. The findings in Science Translational Medicine suggest that norepinephrine may be the missing mechanism in Alzheimer's disease pathology and the reason behind the failure of various Alzheimer's treatments that target beta-amyloid, said senior author Qin Wang.
Study points to possible new mechanism in Alzheimer's pathology
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