ReviewJournal of bioenergetics and biomembranes2010
Mitochondrial functional alterations in relation to pathophysiology of Huntington's disease.
Review in Journal of bioenergetics and biomembranes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
- Oxytocin Prevents the Development of 3-NP-Induced Anxiety and Depression in Male and Female Rats: Possible Interaction of OXTR and mGluR2.Cellular and molecular neurobiology · 2022Article
- New label-free methods for protein relative quantification applied to the investigation of an animal model of Huntington Disease.PloS one · 2020Article
- Huntington's disease: the coming of age.Journal of genetics · 2018Review
- The Association of VDAC with Cell Viability of PC12 Model of Huntington's Disease.Frontiers in oncology · 2016Article
- Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel.Biochimica et biophysica acta · 2013Review
- Degeneration of the cerebellum in Huntington's disease (HD): possible relevance for the clinical picture and potential gateway to pathological mechanisms of the disease process.Brain pathology (Zurich, Switzerland) · 2013Article
- Cell signaling and mitochondrial dynamics: Implications for neuronal function and neurodegenerative disease.Neurobiology of disease · 2013Review
- Distribution of GABAergic interneurons and dopaminergic cells in the functional territories of the human striatum.PloS one · 2012Article
- Mitochondria: the next (neurode)generation.Neuron · 2011Review
- The importance of integrating basic and clinical research toward the development of new therapies for Huntington disease.The Journal of clinical investigation · 2011Review
- Mitochondrial matters in Huntington disease.Journal of bioenergetics and biomembranes · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease which is characterized by psychiatric symptoms, involuntary choreiform movements and dementia with maximum degeneration occurring in striatum and cerebral cortex. Several studies implicate mitochondrial dysfunction to the selective neurodegeneration happening in this disorder. Calcium buffering imbalance and oxidative stress in the mitochondria, critically impaired movement across axons and abnormal fission or fusion of this organelle in the cells are some of the salient features that results in the loss of mitochondrial electron transport chain (ETC) complex function in HD. Although several models involving mutant huntingtin, excitotoxins and mitochondrial complex-II inhibitors have been used to explore the disease, it is not clear how disturbances in mitochondrial functioning is associated with such selective neurodegeneration, or in the expression of huntingtonian phenotypes in animals or man. We have carefully assessed various mitochondrial abnormalities observed in human patient samples, postmortem HD brains, cellular, vertebrate and invertebrate models of the disease, to conclude that ETC dysfunction is an integral part of the disease and justify a causal role of mitochondrial ETC dysfunction for the genesis of this disorder.
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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.