ArticleInternational neurourology journal2019
Dysfunctional Mitochondrial Bioenergetics and Synaptic Degeneration in Alzheimer Disease.
Article in International neurourology journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Bisphenol-A impairs hippocampal neurogenesis by disrupting kinesin-1-dependent mitochondrial trafficking.The Journal of biological chemistry · 2026Article
- Mechanistic insights into the synaptic damage-repair and regeneration processes in neurodegenerative Alzheimer's disease: phytochemicals as neuroprotective agents.Frontiers in synaptic neuroscience · 2026Review
- Synaptic mitochondrial dysfunction and Alzheimer's disease: from molecular mechanisms to therapeutic strategies.Frontiers in pharmacology · 2026Review
- Proteome-Based Biomarkers for Alzheimer's Disease: Old Acquisitions and Innovative Proposals.International journal of molecular sciences · 2025Review
- Atomoxetine Drug Properties for Repurposing as a Candidate Alzheimer's Disease Therapeutic Agent.ACS pharmacology & translational science · 2025Review
- Identification of cuproptosis-related genes in Alzheimer's disease based on bioinformatic analysis.European journal of medical research · 2024Article
- Integrating Mitochondrial Biology into Innovative Cell Therapies for Neurodegenerative Diseases.Brain sciences · 2024Review
- Presenilin2 D439A Mutation Induces Dysfunction of Mitochondrial Fusion/Fission Dynamics and Abnormal Regulation of GTPase Activity.Molecular neurobiology · 2024Article
- Research Progress on Effects of Ginsenoside Rg2 and Rh1 on Nervous System and Related Mechanisms.Molecules (Basel, Switzerland) · 2023Review
- Novel therapeutic strategies targeting mitochondria as a gateway in neurodegeneration.Neural regeneration research · 2023Review
- Protective effect of resveratrol on mitochondrial biogenesis during hyperoxia-induced brain injury in neonatal pups.BMC neuroscience · 2023Article
- Downregulation of Sirtuin 1 Does Not Account for the Impaired Long-Term Potentiation in the Prefrontal Cortex of Female APPswe/PS1dE9 Mice Modelling Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Chemobrain: An accelerated aging process linking adenosine AInternational review of neurobiology · 2023Review
- Energy Crisis Links to Autophagy and Ferroptosis in Alzheimer's Disease: Current Evidence and Future Avenues.Current neuropharmacology · 2023Article
- Decoding the Synaptic Proteome with Long-Term Exposure to Midazolam during Early Development.International journal of molecular sciences · 2022Article
- Electroacupuncture Attenuates Learning and Memory Impairment via PI3K/Akt Pathway in an AmyloidEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Identification and immunological characterization of cuproptosis-related molecular clusters in Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Review
- Instability in NADeLife · 2021Article
- Neonatal Rotenone Administration Induces Psychiatric Disorder-Like Behavior and Changes in Mitochondrial Biogenesis and Synaptic Proteins in Adulthood.Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Synapses are sites of high energy demand which are dependent on high levels of mitochondrial derived adenosine triphosphate. Mitochondria within synaptic structures are key for maintenance of functional neurotransmission and this critical biological process is modulated by energy metabolism, mitochondrial distribution, mitochondrial trafficking, and cellular synaptic calcium flux. Synapse loss is presumed to be an early yet progressive pathological event in Alzheimer disease (AD), resulting in impaired cognitive function and memory loss which is particularly prevalent at later stages of disease. Supporting evidence from AD patients and animal models suggests that pathological mitochondrial dynamics indeed occurs early and is highly associated with synaptic lesions and degeneration in AD neurons. This review comprehensively highlights recent findings that describe how synaptic mitochondria pathology involves dysfunctional trafficking of this organelle, to maladaptive epigenetic contributions affecting mitochondrial function in AD. We further discuss how these negative, dynamic alterations impact synaptic function associated with AD. Finally, this review explores how antioxidant therapeutic approaches targeting mitochondria in AD can further clinical research and basic science investigations to advance our in-depth understanding of the pathogenesis of AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.