Disruption of mitochondrial dynamics in tauopathy

Alzheimer's disease (AD) is characterized pathologically by proteinaceous aggregates composed primarily of Amyloid β (Aβ) and tau. Diseases characterized by abnormal deposition of tau are collectively termed "tauopathies." Aβ acts upstream of tau in the AD pathogenesis pathway, but tau expression is required for the neurodegenerative effects of Aβ. Mitochondrial abnormalities have been documented in Alzheimer's disease and related tauopathies, but the causal relationship between mitochondrial changes and neurodegeneration, as well as specific mechanisms promoting mitochondrial dysfunction, are unclear. Mitochondrial morphology is regulated by fission and fusion events within and between individual mitochondria, and misregulation of this process has been observed in several neurodegenerative diseases. The contribution of mitochondrial dynamics to Alzheimer's disease pathogenesis has not yet been determined.