ReviewiScience2022
Mitochondrial protein synthesis and the bioenergetic cost of neurodevelopment.
Review in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Distinct Mitochondrial Central Dogma Gene Expression in the Buffalo Brain: A Comparative Transcriptomic Study with Metabolically Active Organs.Molecular neurobiology · 2026Article
- Nicotinamide counteracts Rotenone-induced mitochondrial and neuronal dysfunction in a translational early-life model.Scientific reports · 2026Article
- A primer on copper biology in the brain.Neurobiology of disease · 2025Review
- Adaptive protein synthesis in genetic models of copper deficiency and childhood neurodegeneration.Molecular biology of the cell · 2025Article
- Adaptive protein synthesis in genetic models of copper deficiency and childhood neurodegeneration.bioRxiv : the preprint server for biology · 2024Article
- Brain development and bioenergetic changes.Neurobiology of disease · 2024Review
- Splicing-specific transcriptome-wide association uncovers genetic mechanisms for schizophrenia.American journal of human genetics · 2024Article
- Article
- Systemic proteome phenotypes reveal defective metabolic flexibility in Mecp2 mutants.Human molecular genetics · 2023Article
- Mitochondrial proteins encoded by the 22q11.2 neurodevelopmental locus regulate neural stem and progenitor cell proliferation.Molecular psychiatry · 2023Article
- Systemic Proteome Phenotypes Reveal Defective Metabolic Flexibility in Mecp2 Mutants.bioRxiv : the preprint server for biology · 2023Article
- Actin cytoskeletal dynamics do not impose an energy drain on growth cone bioenergetics.Journal of cell science · 2023Article
- Brain Mitochondrial Bioenergetics in Genetic Neurodevelopmental Disorders: Focus on Down, Rett and Fragile X Syndromes.International journal of molecular sciences · 2023Review
- Mitochondrial genes in the 22q11.2 deleted region regulate neural stem and progenitor cell proliferation.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human brain consumes five orders of magnitude more energy than the sun by unit of mass and time. This staggering bioenergetic cost serves mostly synaptic transmission and actin cytoskeleton dynamics. The peak of both brain bioenergetic demands and the age of onset for neurodevelopmental disorders is approximately 5 years of age. This correlation suggests that defects in the machinery that provides cellular energy would be causative and/or consequence of neurodevelopmental disorders. We explore this hypothesis from the perspective of the machinery required for the synthesis of the electron transport chain, an ATP-producing and NADH-consuming enzymatic cascade. The electron transport chain is constituted by nuclear- and mitochondrial-genome-encoded subunits. These subunits are synthesized by the 80S and the 55S ribosomes, which are segregated to the cytoplasm and the mitochondrial matrix, correspondingly. Mitochondrial protein synthesis by the 55S ribosome is the rate-limiting step in the synthesis of electron transport chain components, suggesting that mitochondrial protein synthesis is a bottleneck for tissues with high bionergetic demands. We discuss genetic defects in the human nuclear and mitochondrial genomes that affect these protein synthesis machineries and cause a phenotypic spectrum spanning autism spectrum disorders to neurodegeneration during neurodevelopment. We propose that dysregulated mitochondrial protein synthesis is a chief, yet understudied, causative mechanism of neurodevelopmental and behavioral disorders.
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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 Socratic graph.