Damaged mitochondria coincide with presynaptic vesicle loss and abnormalities in alzheimer's disease brain.

ABSTRACT: Loss of synapses is the most robust pathological correlate of Alzheimer's disease (AD)-associated cognitive deficits, although the underlying mechanism remains incompletely understood. Synaptic terminals have abundant mitochondria which play an indispensable role in synaptic function through ATP provision and calcium buffering. Mitochondrial dysfunction is an early and prominent feature in AD which could contribute to synaptic deficits. Here, using electron microscopy, we examined synapses with a focus on mitochondrial deficits in presynaptic axonal terminals and dendritic spines in cortical biopsy samples from clinically diagnosed AD and age-matched non-AD control patients. Synaptic vesicle density within the presynaptic axon terminals was significantly decreased in AD cases which appeare

SUBMITTER: Wang W 

PROVIDER: S-EPMC10067183 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature