ReviewCNS neuroscience & therapeutics2024
Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer's disease.
Review in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Multi-omics and electrophysiological examination of GABAMolecular psychiatry · 2026Article
- The gut-brain-mitochondria axis in type 2 diabetes-associated cognitive decline: mechanistic convergence, biomarkers, and therapeutic opportunities.Acta diabetologica · 2026Review
- Mitochondrial-Epigenetic Crosstalk in Autism Spectrum Disorder: Linking Cellular Stress to Synaptic Dysfunction and Treatment Resistance.Molecular neurobiology · 2026Review
- High-Altitude Hypoxia Activates JNK-p53 Signaling: Linking Hippocampal Energy Crisis to Cognitive Impairment.CNS neuroscience & therapeutics · 2026Article
- Metabolism Controls the Timing of Human Brain Development and Maturation.Journal of inherited metabolic disease · 2026Review
- The Drp1-CoQ10-Coa6-ETC axis represents a therapeutic potential for working memory impairment caused by neuronal mitochondrial dysfunction.Translational neurodegeneration · 2026Article
- Mitochondrial dysfunction in neonatal brain injury: from molecular mechanisms to therapeutic interventions.Journal of translational medicine · 2026Review
- GLP-1 and the brain's powerhouse: a new perspective on the role of mitochondria in neuroprotection.Metabolic brain disease · 2026Review
- Targeting oxidative stress and neurodegeneration: the role of Putranjiva roxburghii in Alzheimer's.Inflammopharmacology · 2026Review
- Mitochondrial-targeted actions of lycopene: evidence, mechanisms and future directions.Frontiers in pharmacology · 2026Review
- Mitochondrial dysfunction in perimenopausal mood disorders: From hormonal shifts to neuroenergetic failure (Review).International journal of molecular medicine · 2025Review
- Irisin-Treg crosstalk: unveiling a mechanism in neural cognitive regulation.Annals of medicine · 2025Review
- Dexmedetomidine protects against postoperative neurocognitive disorder by mitigating mitochondrial dysfunction through regulating the IP3R-GRP75-VDAC1 complex-mediated calcium transport.Immunologic research · 2025Article
- Convergent and Divergent Mitochondrial Pathways as Causal Drivers and Therapeutic Targets in Neurological Disorders.Current issues in molecular biology · 2025Article
- Serum NPTX2 and cognitive impairment in geriatric diabetes.Biomolecules & biomedicine · 2025Article
- Downregulation of USP9X in the DG Region of the Hippocampus Leads to AD-Like Cognitive Dysfunction in Mice.CNS neuroscience & therapeutics · 2025Article
- Review
- Ultrasound-Induced Synchronized Neural Activities at 40 Hz and 200 Hz Entrained Corresponded Oscillations and Improve Alzheimer's Disease Memory.CNS neuroscience & therapeutics · 2025Article
- Transcriptomic Alteration in the Brain and Gut of Offspring Following Prenatal Exposure to Corticosterone.Experimental neurobiology · 2025Article
- Mitofilin-mtDNA Axis Mediates Chronic Lead Exposure-Induced Synaptic Plasticity Impairment of Hippocampal and Cognitive Deficits.Biomolecules · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic plasticity is believed to underlie the cellular and molecular basis of memory formation. Mitochondria are one of the main organelles involved in metabolism and energy maintenance as plastic organelles that change morphologically and functionally in response to cellular needs and regulate synaptic function and plasticity through multiple mechanisms, including ATP generation, calcium homeostasis, and biogenesis. An increased neuronal activity enhances synaptic efficiency, during which mitochondria's spatial distribution and morphology change significantly. These organelles build up in the pre-and postsynaptic zones to produce ATP, which is necessary for several synaptic processes like neurotransmitter release and recycling. Mitochondria also regulate calcium homeostasis by buffering intracellular calcium, which ensures proper synaptic activity. Furthermore, mitochondria in the presynaptic terminal have distinct morphological properties compared to dendritic or postsynaptic mitochondria. This specialization enables precise control of synaptic activity and plasticity. Mitochondrial dysfunction has been linked to synaptic failure in many neurodegenerative disorders, like Alzheimer's disease (AD). In AD, malfunctioning mitochondria cause delays in synaptic vesicle release and recycling, ionic gradient imbalances, and mostly synaptic failure. This review emphasizes mitochondrial plasticity's contribution to synaptic function. It also explores the profound effect of mitochondrial malfunction on neurodegenerative disorders, focusing on AD, and provides an overview of how they sustain cellular health under normal conditions and how their malfunction contributes to neurodegenerative diseases, highlighting their potential as a therapeutic target for such conditions.
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