ArticleMolecular neurobiology2012
Effect of pesticides on the aggregation of mutant huntingtin protein.
Article in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Who cites it
6 citing papers in PubMed.
- Article
- Caffeic acid recarbonization: A green chemistry, sustainable carbon nano material platform to intervene in neurodegeneration induced by emerging contaminants.Environmental research · 2023Article
- Nanozyme-Participated Biosensing of Pesticides and Cholinesterases: A Critical Review.Biosensors · 2021Review
- The Impact of Environmental Factors on Monogenic Mendelian Diseases.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Flavonoids: Potential Candidates for the Treatment of Neurodegenerative Disorders.Biomedicines · 2021Review
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
The classical reports on neurodegeneration concentrate on studying disruption of signalling cascades. Although it is now well recognized that misfolding and aggregation of specific proteins are associated with a majority of these diseases, their role in aggravating the symptoms is not so well understood. Huntington's disease (HD) is a neurodegenerative disorder that results from damage to complex II of mitochondria. In this work, we have studied the effect of mitochondrial complex I inhibitors, viz. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and rotenone, and complex II inhibitor, viz. 3-nitropropionic acid, on the aggregation of mutant huntingtin (mthtt) protein, whose misfolding and aggregation results in cellular abnormalities characteristic of HD. All three inhibitors were found to accelerate the aggregation of mthtt in vitro, although the amounts of aggregates formed were different in all cases. Thus, apart from their effect on mitochondrial viability, these neurotoxins are capable of interfering with the protein aggregation process and thus, hastening the onset of the disease.
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Registered trials
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