Pathophysiology and Potential Targets of Neural Repair
The pathophysiology of AD is very complex. Aβ plaques, and NFTs are the main neuropathological hallmarks. Senile Aβ
plaques are important pathophysiological changes seen in AD and thus form the essential component of the “amyloid
hypothesis. This hypothesis proposes that the deposition of Aβ plaques precedes and induces the neuronal abnormalities that underlie the development of dementia.[4] In AD, the soluble form of Aβ has toxic effects on the neurons, including increasing the oxidative stress, precipitating the programmed cell death and lowering the cell injury threshold.[5] NFTs are dense intracellular protein deposits that are composed of the normal cytoskeletal protein, tau. The formation of NFTs in neurons is associated with extensive phosphorylation and cross‑linking of the tau molecules.
However, the initiating event is not well understood.[6] Many of the therapeutic strategies in AD, including neuro‑restorative strategies to be discussed below, depend on treating the above mentioned mechanisms, especially decreasing the Aβ deposits. However, the pathophysiology of AD involves multiple mechanisms, that are at present, not well understood.