On the central role of mitochondria dysfunction and oxidative stress in Alzheimer's disease

BackgroundAlzheimer's disease (AD) is the commonest cause of dementia, with approximately 5 million new cases occurring annually. Despite decades of research, its complex pathophysiology and etiopathogenesis presents a major hindrance to the development of an effective treatment and prevention strategy. Aging is the biggest risk factor for the development of AD, and the total number of older people in the population is going to significantly increase in the next decades, suggesting that AD incidence and prevalence is likely to increase in the future. This makes the need for a better understanding of the disease to be extremely urgent.MethodsA search was done by accessing PubMed/Medline, EBSCO, and PsycINFO databases. The search string used was (dementia* OR Alzheimer's) AND (pathophysiology* OR pathogenesis). New key terms were identified (new term included vitamin D, thyroid hormone, mitochondria dysfunction, oxidative stress, testosterone, estrogen, melatonin, progesterone, luteinizing hormone, amyloid-beta (A beta), and hyperphosphorylated tau). The electronic databases were searched for titles or abstracts containing these terms in all published articles between January 1, 1965, and January 31, 2019. The search was limited to studies published in English and other languages involving both animal and human subjects.ResultsMitochondria dysfunction and oxidative stress play a critical role in AD etiopathogenesis and pathophysiology.ConclusionAD treatment and prevention strategies must be geared towards improving mitochondrial function and attenuating oxidative stress.