Cited by 211Alzheimer's disease research and treatmentsMitochondrial Function and PathologyNeuroscience and Neuropharmacology Research

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Mitochondrial Dysfunction and Synaptic Transmission Failure in Alzheimer’s Disease

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Guo, Lan, Tian, Jing, Du, Heng·2017·Journal of Alzheimer’s Disease

DOI 10.3233/jad-160702PMC PMC5605817

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Abstract

Alzheimer’s disease (AD) is a chronic neurodegenerative disorder, in which multiple risk factors converge. Despite the complexity of the etiology of the disease, synaptic failure is the pathological basis of cognitive impairment, the cardinal sign of AD. Decreased synaptic density, compromised synaptic transmission, and defected synaptic plasticity are hallmark synaptic pathologies accompanying AD. However, the mechanisms by which synapses are injured in AD-related conditions have not been fully elucidated. Mitochondria are a critical organelle in neurons. The pivotal role of mitochondria in supporting synaptic function and the concomitant occurrence of mitochondrial dysfunction with synaptic stress in postmortem AD brains as well as AD animal models seem to lend the credibility to the hypothesis that mitochondrial defects underlie synaptic failure in AD. This concept is further strengthened by the protective effect of mitochondrial medicine on synaptic function against the toxicity of amyloid-β, a key player in the pathogenesis of AD. In this review, we focus on the association between mitochondrial dysfunction and synaptic transmission deficits in AD. Impaired mitochondrial energy production, deregulated mitochondrial calcium handling, excess mitochondrial reactive oxygen species generation and release play a crucial role in mediating synaptic transmission deregulation in AD. The understanding of the role of mitochondrial dysfunction in synaptic stress may lead to novel therapeutic strategies for the treatment of AD through the protection of synaptic transmission by targeting to mitochondrial deficits.

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Authors: Guo, L., Tian, J., & Du, H.
Affiliations: The University of Texas at Dallas (US)
Shandong University (CN)
Corresponding author: Du, Heng
ORCID: Guo, Lan
Tian, Jing
Du, Heng
Venue: Journal of Alzheimer’s Disease
Publisher: SAGE Publications
Published: 2016-09-20
Volume: 57
Issue: 4
Pages: 1071-1086
ISSN: 1387-2877 (ISSN-L)
1875-8908
DOI: 10.3233/jad-160702
PMC: PMC5605817
OpenAlex: W2522744939
Cited by: 211
References: 243
Citations by year: 2026: 26 · 2025: 31 · 2024: 29 · 2023: 31 · 2022: 22 · 2021: 22 · 2020: 28 · 2019: 17 · 2018: 3 · 2017: 2
FWCI: 0.86
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Journal of Alzheimer s Disease (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (R00AG037716, R01AG053588)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: Alzheimer's disease, mitochondrial dysfunction
MeSH terms: Alzheimer Disease, Animals, Humans, Mitochondria, Synaptic Transmission, Mitochondrial Diseases

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Mitochondrial Dysfunction and Synaptic Transmission Failure in Alzheimer’s Disease

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