Table 1. Some Targets of Action of Amyloid β and Tau Impairment Due to Oxidative Distress^a.

amyloid β peptide	tau	genetics
downregulation of the GluN1 subunit of NMDAR receptors	accumulation of Cdc2/cyclin B1 kinase, leading to cell cycle re-entry	ApoE
endocytosis of EphB2 class of tyrosine kinases	interaction with Aβ leading to activation of IL-1b and neuroninflammation	BACE
upregulation of apoptosin, a mitochondrial protein, leading to mitochondrial dysfunction and neurotoxicity	activation of ERK2, NFkb, p38, etc. leading to hyperphosphorylation of tau	PSEN1
interaction with metals (e.g., Fe, Cu, Zn) leading to Aβ deposition
downregulation of COX activity on interaction with heme

^aGenetic studies have shown AD-related genes (APOE, PSEN1, and BASE) to be related to Aβ deposition.^62,63 Additionally, other targets leading up to Aβ deposition or a consequence of the same involve N-methyl-D-aspartate (NMDAR) receptors,⁶⁴ EphB2 tyrosine kinases,⁶⁵ metal interaction,⁴² etc. Oxidative stress can affect tau by reconfiguring cell cycle checkpoints,⁶⁶ neuroinflammatory mechanisms,⁶⁷ and other factors that lead to hyperphosphorylation of the protein.