Abstract
AbstractNeurofibrillary tangles composed of tau protein and senile plaque accumulated by amyloid‐β (Aβ) are two hallmarks in Alzheimer disease (AD). In the patients with AD, tau is abnormally hyperphosphorylated, mutated or misfolding, which endows tau with stronger tendency to aggregate. Tau protein has the potency to mediate neuron toxicity of Aβ. The reduction of tau level ameliorates degeneration of neuron axon. Therefore, many researches are exploring new methods to regulate tau level. This review will mainly focus on small molecules that can directly inhibit tau fibrillation or control tau accumulation by regulating tau phosphorylation process.
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