ArticleBiochimica et biophysica acta2010
Age-related deficiencies in complex I endogenous substrate availability and reserve capacity of complex IV in cortical neuron electron transport.
Article in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Breaking the age-related redox spiral for regeneration.Neural regeneration research · 2026Article
- Mechanisms of Brain Aging and Their Links to Alzheimer's and Parkinson's Disease Pathology.International journal of molecular sciences · 2026Review
- Age-Related Intraneuronal Aggregation of Amyloid-β in Endosomes, Mitochondria, Autophagosomes, and Lysosomes.Journal of Alzheimer's disease : JAD · 2020Article
- Physical Activity and Brain Health.Genes · 2019Review
- Age- and AD-related redox state of NADH in subcellular compartments by fluorescence lifetime imaging microscopy.GeroScience · 2019Article
- Global Metabolic Shifts in Age and Alzheimer's Disease Mouse Brains Pivot at NAD+/NADH Redox Sites.Journal of Alzheimer's disease : JAD · 2019Article
- Organ reserve, excess metabolic capacity, and aging.Biogerontology · 2018Review
- Recurrent Sleep Fragmentation Induces Insulin and Neuroprotective Mechanisms in Middle-Aged Flies.Frontiers in aging neuroscience · 2016Article
- Article
- A reversible early oxidized redox state that precedes macromolecular ROS damage in aging nontransgenic and 3xTg-AD mouse neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Article
- High-level inhibition of mitochondrial complexes III and IV is required to increase glutamate release from the nerve terminal.Molecular neurodegeneration · 2011Article
- Age-Induced Alterations in Hippocampal Function and Metabolism.Aging and disease · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Respiratory enzyme complex dysfunction is mechanistically involved in mitochondrial failure leading to neurodegenerative disease, but the pathway is unclear. Here, age-related differences in mitochondrial respiration were measured in both whole and permeabilized neurons from 9-month and 24-month adult rat cortex cultured in common conditions. After permeabilization, respiration increased in both ages of neurons with excess substrates. To dissect specific deficiencies in the respiratory chain, inhibitors for each respiratory chain complex were used to isolate their contributions. Relative to neurons from 9-month rats, in neurons isolated from 24-month rats, complexes I, III, and IV were more sensitive to selective inhibition. Flux control point analysis identified complex I in neurons isolated from 24-month rats as the most sensitive to endogenous substrate availability. The greatest age-related deficit in flux capacity occurred at complex IV with a 29% decrease in neurons isolated from 24-month rats relative to those from 9-month rats. The deficits in complexes I and III may contribute to a redox shift in the quinone pool within the electron transport chain, further extending these age-related deficits. Together these changes could lead to an age-related catastrophic decline in energy production and neuronal death.
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Registered trials
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