Mitochondrial Dysfunction-Mediated Neurodegeneration in Alzheimer's Disease

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This hypothesis proposes that mitochondrial dysfunction represents a primary pathogenic mechanism in Alzheimer's disease, operating through impaired ATP synthesis and increased oxidative stress that precedes and drives amyloid-beta accumulation. Specifically, mutations or age-related damage to TFAM (Transcription Factor A, Mitochondrial) lead to defective mitochondrial DNA replication and reduced