ArticleCell reports2018
Mitochondrial Aging Defects Emerge in Directly Reprogrammed Human Neurons due to Their Metabolic Profile.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed.
- Protracted Fate Acquisition and Epigenetic De-Aging During Induced Neural Stem Cell Conversion of Human Blood Cells.Aging cell · 2026Article
- Transcriptomic Evidence of Mitochondrial Double-Stranded RNA Accumulation in Brain Aging and Alzheimer's Disease.Aging cell · 2026Article
- Harnessing Lessons from Gel-Based and Advanced Biomaterial Therapeutics to Enable Direct Cellular Reprogramming.Gels (Basel, Switzerland) · 2026Review
- Article
- Mitochondrial double-stranded RNA accumulation in brain aging and Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Genetic regulators of neuronal survival across metabolic environments.bioRxiv : the preprint server for biology · 2025Article
- Investigating the ageing-Parkinson's disease nexus: standardisation of in vitro models and techniques by the PD-AGE network.NPJ Parkinson's disease · 2025Review
- Cellular Models of Aging and Senescence.Cells · 2025Review
- The complex web of membrane contact sites in brain aging and neurodegeneration.Cellular and molecular life sciences : CMLS · 2025Review
- Tracing mitochondrial marks of neuronal aging in iPSCs-derived neurons and directly converted neurons.Communications biology · 2025Article
- Mitochondrial dynamics and bioenergetics in Alzheimer's induced pluripotent stem cell-derived neurons.Brain : a journal of neurology · 2025Article
- Direct fibroblast reprogramming: an emerging strategy for treating organic fibrosis.Journal of translational medicine · 2025Review
- Fate erasure logic of gene networks underlying direct neuronal conversion of somatic cells by microRNAs.Cell reports · 2025Article
- Review
- Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes.International journal of molecular sciences · 2024Article
- Human iPSCs from Aged Donors Retain Their Mitochondrial Aging Signature.International journal of molecular sciences · 2024Article
- Age-specific and compartment-dependent changes in mitochondrial homeostasis and cytoplasmic viscosity in mouse peripheral neurons.Aging cell · 2024Article
- Harnessing BDNF Signaling to Promote Resilience in Aging.Aging and disease · 2024Review
- In vitro human cell culture models in a bench-to-bedside approach to epilepsy.Epilepsia open · 2024Review
- Physiological aging and inflammation-induced cellular senescence may contribute to oligodendroglial dysfunction in MS.Acta neuropathologica · 2024Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
Mitochondria are a major target for aging and are instrumental in the age-dependent deterioration of the human brain, but studying mitochondria in aging human neurons has been challenging. Direct fibroblast-to-induced neuron (iN) conversion yields functional neurons that retain important signs of aging, in contrast to iPSC differentiation. Here, we analyzed mitochondrial features in iNs from individuals of different ages. iNs from old donors display decreased oxidative phosphorylation (OXPHOS)-related gene expression, impaired axonal mitochondrial morphologies, lower mitochondrial membrane potentials, reduced energy production, and increased oxidized proteins levels. In contrast, the fibroblasts from which iNs were generated show only mild age-dependent changes, consistent with a metabolic shift from glycolysis-dependent fibroblasts to OXPHOS-dependent iNs. Indeed, OXPHOS-induced old fibroblasts show increased mitochondrial aging features similar to iNs. Our data indicate that iNs are a valuable tool for studying mitochondrial aging and support a bioenergetic explanation for the high susceptibility of the brain to aging.
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