ReviewMechanisms of ageing and development2017
The chicken or the egg: mitochondrial dysfunction as a cause or consequence of toxicity in Huntington's disease.
Review in Mechanisms of ageing and development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
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
19 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Mitochondria Metabolism Regulates Glucose-Lipid Homeostasis in Neurodegenerative Diseases.Research (Washington, D.C.) · 2025Review
- Complex II ambiguities-FADHThe Journal of biological chemistry · 2024Review
- Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.International journal of molecular sciences · 2023Review
- Predicting Mitochondrial Dynamic Behavior in Genetically Defined Neurodegenerative Diseases.Cells · 2022Review
- A Double-Pronged Sword: XJB-5-131 Is a Suppressor of Somatic Instability and Toxicity in Huntington's Disease.Journal of Huntington's disease · 2022Review
- XJB-5-131 Is a Mild Uncoupler of Oxidative Phosphorylation.Journal of Huntington's disease · 2022Article
- Hyperbaric Oxygen Treatment: Effects on Mitochondrial Function and Oxidative Stress.Biomolecules · 2021Review
- Brain Region and Cell Compartment Dependent Regulation of Electron Transport System Components in Huntington's Disease Model Mice.Brain sciences · 2021Article
- Accelerated expansion of pathogenic mitochondrial DNA heteroplasmies in Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Impaired response of cerebral oxygen metabolism to visual stimulation in Huntington's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Bioenergetic deficits in Huntington's disease iPSC-derived neural cells and rescue with glycolytic metabolites.Human molecular genetics · 2020Article
- Expression of mutant exon 1 huntingtin fragments in human neural stem cells and neurons causes inclusion formation and mitochondrial dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Energy Metabolism and Mitochondrial Superoxide Anion Production in Pre-symptomatic Striatal Neurons Derived from Human-Induced Pluripotent Stem Cells Expressing Mutant Huntingtin.Molecular neurobiology · 2020Article
- Metabolic Reprogramming in Astrocytes Distinguishes Region-Specific Neuronal Susceptibility in Huntington Mice.Cell metabolism · 2019Article
- Brain mitochondrial iron accumulates in Huntington's disease, mediates mitochondrial dysfunction, and can be removed pharmacologically.Free radical biology & medicine · 2018Article
- Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases.Cell death and differentiation · 2018Review
- Oxidative metabolism and CaNeurochemistry international · 2017Article
- Comparison of Sirtuin 3 Levels in ALS and Huntington's Disease-Differential Effects in Human Tissue Samples vs. Transgenic Mouse Models.Frontiers in molecular neuroscience · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction and ensuing oxidative damage is typically thought to be a primary cause of Huntington's disease, Alzheimer's disease, and Parkinson disease. There is little doubt that mitochondria (MT) become defective as neurons die, yet whether MT defects are the primary cause or a detrimental consequence of toxicity remains unanswered. Oxygen consumption rate (OCR) and glycolysis provide sensitive and informative measures of the functional status MT and the cells metabolic regulation, yet these measures differ depending on the sample source; species, tissue type, age at measurement, and whether MT are measured in purified form or in a cell. The effects of these various parameters are difficult to quantify and not fully understood, but clearly have an impact on interpreting the bioenergetics of MT or their failure in disease states. A major goal of the review is to discuss issues and coalesce detailed information into a reference table to help in assessing mitochondrial dysfunction as a cause or consequence of Huntington's disease.
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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.