The formation of PHFs and deposits of NFTs in the cytosol may physically obstruct the movement of mitochondria along microtubules or inhibit fast axonal transport by triggering the release of cargo from the kinesin [84]; and (4) Dysfunctional tau increases the susceptibility of neurons to Aβ and excitotoxic insults, such as the excessive activation of glutamate receptors, supporting tau as a downstream mediator of Aβ-induced toxicity in AD [85,86]. The gene discussed is MAPT; the disease is Alzheimer disease.