Figure 1.

Schematic representation of a complex interplay between abnormal amyloid-beta (Aβ) and tau proteins leading to neuroinflammation and neurodegeneration in Alzheimer’s disease (AD).

Aβ aggregates into plaques outside the neurons, while abnormal tau proteins accumulate inside the neurons in specific regions of the brain involved in spatial learning and memory. After accumulation of Aβ plaques occurs significantly, the abnormal tau proteins spread rapidly throughout the brain leading to significant neuroinflammation, neurodegeneration, and cognitive deficits in AD.