ArticleActa neuropathologica communications2023
Damaged mitochondria coincide with presynaptic vesicle loss and abnormalities in alzheimer's disease brain.
Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 43 citations in OpenAlex.
- Mitochondrial dynamics in environmental neurotoxicity: beyond oxidative stress toward spatial and functional reorganization.Archives of toxicology · 2026Review
- Estrogen Withdrawal-Induced Cognitive Impairment in Menopausal Women: Mechanisms and Prospects for Integrated Interventions.International journal of molecular sciences · 2026Review
- Article
- Hippocampal CA1 and CA2 dendritic compartment-specific differences in mitochondrial form and function.Progress in neurobiology · 2026Article
- Synaptic mitochondria in aging and neurodegenerative diseases: Functional decline and vulnerability.Neural regeneration research · 2026Article
- Disrupted lipid homeostasis as a pathogenic mechanism in ABCA7-associated Alzheimer's disease risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Nanomolar Cadmium Disrupts Neurotransmitter Release Timing via a ROS-dependent Mechanism at the Mouse Neuromuscular Junction: Modulation by Nanomolar ZnNeurochemical research · 2026Article
- Region-specific ups and downs in mitochondrial numerical densities during Alzheimer's disease progression: A pilot study in human brains.Journal of Alzheimer's disease : JAD · 2026Article
- Digging Deep into Alzheimer Disease: How Electron Microscopy Helps Elucidating Its Pathogenesis.Cellular and molecular neurobiology · 2026Review
- The dual face of human chorionic gonadotropin in the CNS: neuroprotection, signaling, and possible pathological effects.Archives of gynecology and obstetrics · 2026Review
- Mitochondrial CaNature metabolism · 2026Article
- Synaptic mitochondrial dysfunction and Alzheimer's disease: from molecular mechanisms to therapeutic strategies.Frontiers in pharmacology · 2026Review
- Recent molecular insights and biosensor-based diagnostic technologies for hyperphosphorylated Tau in Alzheimer's disease.Alzheimer's research & therapy · 2025Review
- Hippocampal cell- and circuit-specific differences in mitochondrial form and function.bioRxiv : the preprint server for biology · 2025Article
- Polarized ATP synthase in synaptic mitochondria induced by learning and plasticity signals.Communications biology · 2025Article
- Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease.The Journal of physiology · 2025Review
- Microglia-mediated inflammation and synaptic pruning contribute to sleep deprivation-induced mania in a sex-specific manner.Translational psychiatry · 2025Article
- Microvesicles carrying EV71 virions cross BBB through endocytic pathway to induce brain injury.Cell communication and signaling : CCS · 2025Article
- Synaptic Vesicle-Related Proteins and Ubiquilin 2 in Cortical Synaptosomes Mediate Cognitive Impairment in Vascular Dementia Rats.Molecular neurobiology · 2025Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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 appeared largely due to significantly decreased reserve pool, but there were significantly more presynaptic axons containing enlarged synaptic vesicles or dense core vesicles in AD. Importantly, there was reduced number of mitochondria along with significantly increased damaged mitochondria in the presynapse of AD which correlated with changes in SV density. Mitochondria in the post-synaptic dendritic spines were also enlarged and damaged in the AD biopsy samples. This study provided evidence of presynaptic vesicle loss as synaptic deficits in AD and suggested that mitochondrial dysfunction in both pre- and post-synaptic compartments contribute to synaptic deficits in AD.
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