Alzheimer's disease (AD) is a neurodegenerative condition that is distinguished by the presence of extracellular amyloid β-fibrillar plaques and intraneuronal tau protein neurofibrillary tangles( NFTs) in the brain. Oxidative stress, one of the earliest events in AD, can elicit tau hyperphosphorylation, which destabilizes microtubules by reducing tau binding affinity. This process leads to the formation of NFTs, which are the primary pathological feature of AD. In Alzheimer's disease patients, tau accumulation is pathologically more closely linked to the development of cognitive decline and neurodegeneration than Aβ plaques . Tau glycosylation elevates the amyloid protein precursor and releases approximately 4 kD of amyloid peptide . The dysfunction of the autophagy-lysosomal system may also facilitate tau aggregation . In mature AD brains, mitochondria that are structurally defective are present in neurons, capillaries, and astrocytes. In addition to being linked to aging through mitochondrial DNA (mtDNA) mutations and reactive oxygen accumulation . Tau is hyperphosphorylated and dissociated from MTs in AD, which leads to MT instability and impaired axonal transport .