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Amyloid Beta Mediated Mitochondrial Dysfunction in Alzheimer's disease: A Mini Review.

Mitochondria, the sub cellular organelles inside cells transform oxygen and nutrients into adenosine triphosphate (ATP), the main source of fuel for cellular activity and survival. Mitochondria, sustain life through energy transformation and intracellular signaling. Increasing evidence implicates mitochondrial dysfunction induced bioenergetic failure in multiple neurodegenerative disorders including Alzheimer‘s disease (AD). Alzheimer‘s disease is the most tragic geriatric complication that takes away the essence of life. Beside tau hyper phosphorylation, cholinergic dysfunction and neuroinflammation, amyloid β are the prominent pathological markers of the disease. The major target of Aβ is the mitochondrion and these cellular powerhouses differ between Alzheimer's brains and healthy brains. Aβ block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial machinery, disrupt the electron transport system, increase oxidative stress leading to mitochondrial damage and ultimately prevent neurons from functioning normally. This has led to the view that mitochondria play an important role in Alzheimer's, not only as contributors but also as drivers of disease.