ReviewProgress in molecular biology and translational science2012
Biology of mitochondria in neurodegenerative diseases.
Review in Progress in molecular biology and translational science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
81 citing papers in PubMed, 165 citations in OpenAlex.
- Creatine supplementation enhances corticomotor excitability and cognitive performance during oxygen deprivation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Trial
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.PLoS biology · 2025Article
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.bioRxiv : the preprint server for biology · 2025Article
- Exploring the mechanism of metabolic cell death-related genes AKR1C2 and MAP1LC3A as biomarkers in Parkinson's disease.Scientific reports · 2025Article
- Recent advances in nanotechnology for Parkinson's disease: diagnosis, treatment, and future perspectives.Frontiers in medicine · 2025Review
- Cellular Organelle-Related Transcriptomic Profile Abnormalities in Neuronopathic Types of Mucopolysaccharidosis: A Comparison with Other Neurodegenerative Diseases.Current issues in molecular biology · 2024Article
- Healthy mitochondrial DNA in balanced mitochondrial dynamics: A potential marker for neuro‑aging prediction (Review).Biomedical reports · 2023Review
- Copy number analysis from whole-exome sequencing data revealed a novel homozygous deletion inHeliyon · 2023Article
- Neurodegeneration, Mitochondria, and Antibiotics.Metabolites · 2023Review
- Isolated Mitochondrial Preparations andCurrent neuropharmacology · 2023Review
- Homozygous CADPS2 Mutations Cause Neurodegenerative Disease with Lewy Body-like Pathology in Parrots.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- The Antioxidative Effects of Picein and Its Neuroprotective Potential: A Review of the Literature.Molecules (Basel, Switzerland) · 2022Review
- Mitochondrial Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2022Review
- Lipid Nanoparticles: Promising Treatment Approach for Parkinson's Disease.International journal of molecular sciences · 2022Review
- Association of p53 with Neurodegeneration in Parkinson's Disease.Parkinson's disease · 2022Review
- Analysis of Mitochondrial Dysfunction by Microplate Reader in hiPSC-Derived Neuronal Cell Models of Neurodegenerative Disorders.Methods in molecular biology (Clifton, N.J.) · 2022Review
- UsingFrontiers in pharmacology · 2022Review
- Swim Training Ameliorates Hyperlocomotion of ALS Mice and Increases Glutathione Peroxidase Activity in the Spinal Cord.International journal of molecular sciences · 2021Article
- Progressive Mitochondrial SOD1International journal of molecular sciences · 2021Article
- Mitochondrial Protein Import Dysfunction in Pathogenesis of Neurodegenerative Diseases.Molecular neurobiology · 2021Review
21 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
1 author at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) are the most common human adult-onset neurodegenerative diseases. They are characterized by prominent age-related neurodegeneration in selectively vulnerable neural systems. Some forms of AD, PD, and ALS are inherited, and genes causing these diseases have been identified. Nevertheless, the mechanisms of the neuronal degeneration in these familial diseases, and in the more common idiopathic (sporadic) diseases, are unresolved. Genetic, biochemical, and morphological analyses of human AD, PD, and ALS, as well as their cell and animal models, reveal that mitochondria could have roles in this neurodegeneration. The varied functions and properties of mitochondria might render subsets of selectively vulnerable neurons intrinsically susceptible to cellular aging and stress and the overlying genetic variations. In AD, alterations in enzymes involved in oxidative phosphorylation, oxidative damage, and mitochondrial binding of Aβ and amyloid precursor protein have been reported. In PD, mutations in mitochondrial proteins have been identified and mitochondrial DNA mutations have been found in neurons in the substantia nigra. In ALS, changes occur in mitochondrial respiratory chain enzymes and mitochondrial programmed cell death proteins. Transgenic mouse models of human neurodegenerative disease are beginning to reveal possible principles governing the biology of selective neuronal vulnerability that implicate mitochondria and the mitochondrial permeability transition pore. This chapter reviews several aspects of mitochondrial biology and how mitochondrial pathobiology might contribute to the mechanisms of neurodegeneration in AD, PD, and ALS.
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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.