ArticleNeurochemical research2016
Brain cortex mitochondrial bioenergetics in synaptosomes and non-synaptic mitochondria during aging.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 80 citations in OpenAlex.
- Synaptic mitochondria in aging and neurodegenerative diseases: Functional decline and vulnerability.Neural regeneration research · 2026Article
- Dynamic changes in mitochondrial function in brain cortex synaptosomes during aging.Journal of bioenergetics and biomembranes · 2026Article
- Unraveling sex differences in age-related hippocampal decline: differential mitochondrial dysfunction, Lonp1-dependent mitochondrial proteostasis and mtROS production in aged C57BL/6 mice.Cell death & disease · 2025Article
- Identifying a novel Mecp2-mediated epigenetic mechanism controlling Lonp1 in the hippocampus and its disruption by aging.Scientific reports · 2025Article
- Spermidine Enhances Mitochondrial Bioenergetics in Young and Aged Human-Induced Pluripotent Stem Cell-Derived Neurons.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Sulfotransferase 1C2 Increases Mitochondrial Respiration by Converting Mitochondrial Membrane Cholesterol to Cholesterol Sulfate.Biochemistry · 2024Article
- Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Long-Term Region-Specific Mitochondrial Functionality Changes in Both Cerebral Hemispheres after fMCAo Model of Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Axonal energy metabolism, and the effects in aging and neurodegenerative diseases.Molecular neurodegeneration · 2023Review
- Coenzyme QScientific reports · 2023Article
- Isolated Mitochondrial Preparations andCurrent neuropharmacology · 2023Review
- Natural products regulate mitochondrial function in cognitive dysfunction-A scoping review.Frontiers in pharmacology · 2023Article
- Effects of aging and long-term physical activity on mitochondrial physiology and redox state of the cortex and cerebellum of female rats.Physiological reports · 2022Article
- Divergent Cellular Energetics, Glutamate Metabolism, and Mitochondrial Function Between Human and Mouse Cerebral Cortex.Molecular neurobiology · 2022Article
- The compartmentalised nature of neuronal mitophagy: molecular insights and implications.Expert reviews in molecular medicine · 2022Review
- Phosphorylated tau as a toxic agent in synaptic mitochondria: implications in aging and Alzheimer's disease.Neural regeneration research · 2022Review
- Simultaneous Alteration of the Circadian Variation of Memory, Hippocampal Synaptic Plasticity, and Metabolism in a Triple Transgenic Mouse Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2022Article
- Ionizing Radiation-Induced Brain Cell Aging and the Potential Underlying Molecular Mechanisms.Cells · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in mitochondrial bioenergetics have been associated with brain aging. In order to evaluate the susceptibility of brain cortex synaptosomes and non-synaptic mitochondria to aging-dependent dysfunction, male Swiss mice of 3 or 17 months old were used. Mitochondrial function was evaluated by oxygen consumption, mitochondrial membrane potential and respiratory complexes activity, together with UCP-2 protein expression. Basal respiration and respiration driving proton leak were decreased by 26 and 33 % in synaptosomes from 17-months old mice, but spare respiratory capacity was not modified by aging. Succinate supported state 3 respiratory rate was decreased by 45 % in brain cortex non-synaptic mitochondria from 17-month-old mice, as compared with young animals, but respiratory control was not affected. Synaptosomal mitochondria would be susceptible to undergo calcium-induced depolarization in 17 months-old mice, while non-synaptic mitochondria would not be affected by calcium overload. UCP-2 was significantly up-regulated in both synaptosomal and submitochondrial membranes from 17-months old mice, compared to young animals. UCP-2 upregulation seems to be a possible mechanism by which mitochondria would be resistant to suffer oxidative damage during aging.
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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.