Figure 7

Schematic representation of the OKA-induced AD-like pathology and its amelioration by NIR PBM therapy. By selectively inhibiting PP2A, OKA induces hyperphosphorylation of tau and thus its detachment from microtubules, resulting in the formation of toxic tau aggregates and NFTs. Furthermore, our results indicate that OKA induces neuroinflammation, mitochondrial dysfunction, and apoptosis, all together leading to cognitive impairment and AD-like pathology. In contrast, a sequential NIR PBM therapy enhances mitochondrial biogenesis/function, antioxidant and anti-inflammatory defense systems, and pro-survival/cell-proliferation signals by increasing expression of Sirt1, PGC-1α, and TFAM, improving mitochondrial membrane potential (MMP), and increasing production of NO, ATP, antioxidants (e.g., SOD, GSH, CAT), as well as by activating PI3K/AKT, RAS/ERK, PKC, and PKA/Sirt1/PGC-1α signaling pathways. The findings of the present study are depicted as upward red (AD-inducing) and green (AD-ameliorating) arrows.