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Amyloid β is one of the pathological targets in Alzheimer's Disease, the design frame of clinical trials should based on the heterogenicities of AD. Further, as Prof. Murphy said, "Although it may not quite be time to give up on Aβ immunotherapy for treating Alzheimer’s disease, it would be foolish to ignore the continued failures of antiamyloid approaches". The question is:
When is the time to shift the aim of AD treatment from Aβ, or P-tau, to the right therapeutic target of the cognitive synapse network?