The cross-talk between ApoE and Tau protein in Alzheimer's disease

Alzheimer's disease is characterized by two mechanisms, one that occur extracellularly and the other occurs intracellularly. The two most important proteins are extracellular amyloid βeta (Aβ) and intracellular hyperphosphorylated Tau that are contained in senile plaques and neurofibrillary tangles respectively. AD accounts for cognitive impairment and progressive neuronal degeneration eventually, there is significant cerebral atrophy due to neuronal cell death. Initially, there is synaptic damage, synaptic loss plays a strong role in cognitive impairment in patients with AD. Also, evidence suggests that modifications in adult neurogenesis in the hippocampus plays a role in AD. It has been investigated that synaptic pathology and defective neurogenesis in AD are related to progressive accumulation of Aβ oligomers rather than fibrils. Aβ oligomer formation occurs when the APP is cleaved off and subsequently Aβ protein that is generated due to this cleavage is not cleared off by the ApoE mechanism.