Table 1.

The effects of several phytochemicals on mitochondrial dysfunctions in AD pathogenesis.

Phytochemical	Experimental Model	Pathobiology	Molecular Signaling	Research Outcomes	References
Liquiritigenin	Aβ-mediated SK-N-MC cell AD model	Mitochondrial fragmentation	MFN1, MFN2, and OPA1 signaling accumulation	Prevent cytotoxicity and mitochondrial fragmentation	[103]
Genistein	APP/PS1 rat model of sporadic AD	Increased Aβ- and tau protein	Autophagy induction and decreased protein aggregates	Enhanced memory and learning function	[101, 104]
Anthocyanins	APPswe double mutation	Oxidative stress and mitochondrial dysfunction	Improved NADH levels	Increased mitochondrial dysfunction	[105]
Quercetin	Sprague-Dawley rat H2O2-induced neurotoxicity	Oxidative stress	Improved Aβ clearance	Neuroprotection	[106]
Sulfuretin	Aβ neurotoxicity in SH-SY5Y cells and primary hippocampal neurons	Oxidative stress	PI3K/AKT and NRF2/HO activation	Neuroprotection	[107]
Epigallocatechin-3-gallate (EGCG)	Primary cortical rat neurons	Pathological tau species	Improved autophagy and tau clearance	Improved NRF2-dependent tau degradation	[108]
Curcumin	Sprague-Dawley rats	Cerebral ischemia	Improved autophagy by PI3K/AKT/mTOR pathway	Neuroprotection	[109]
Resveratrol	Aβ-induced cytotoxicity in PC12 cells	Oxidative stress	Decreased ROS, activated SOD	Reduced memory impairment and neuroprotection	[110]
Polyphenols	SH-SY5Y neuroblastoma cells	Oxidative stress	Initiation of KEAP1-NRF2 signaling	Neuroprotection	[111]
Kaempferol	Porcine embryos	Oxidative stress	Activated autophagy	Prevented MMP and ROS	[112]