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Despite this mechanistic insight, the clinical assessment of zinc status remains largely confined to systemic measurements, which poorly reflect intracellular distributions or organelle-specific dysfunction

Mitochondrial dysfunctions in AD comprising of oxidative phosphorylation defects, ATP production decrease, reactive oxygen species generation over and above the normal level, poor mitochondrial dynamics, and vacuolar-type H+-ATPase-mediated cell death are the factors that further worsen the situation and hence speed up the process of neuronal death and eventually, disease progression

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