ReviewCellular and molecular life sciences : CMLS2012
Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.
Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 33 citations in OpenAlex.
- Berberine can be a Potential Therapeutic Agent in Treatment of Huntington's Disease: A Proposed Mechanistic Insight.Molecular neurobiology · 2025Review
- Single-cell sequencing reveals a regulatory role of WT1 in mast cell proliferation in endometrial polyps.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Risk factors for cognitive dysfunction and glycemic management in older adults with type 2 diabetes mellitus: a retrospective study.BMC endocrine disorders · 2023Article
- Mutant Presenilin 1 Dysregulates Exosomal Proteome Cargo Produced by Human-Induced Pluripotent Stem Cell Neurons.ACS omega · 2021Article
- Article
- Design and characterization of mutant and wildtype huntingtin proteins produced from a toolkit of scalable eukaryotic expression systems.The Journal of biological chemistry · 2019Article
- Proteostasis in Huntington's disease: disease mechanisms and therapeutic opportunities.Acta pharmacologica Sinica · 2018Review
- Towards an Understanding of Energy Impairment in Huntington's Disease Brain.Journal of Huntington's disease · 2017Review
- Energy Homeostasis and Abnormal RNA Metabolism in Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2017Review
- T1ρ imaging in premanifest Huntington disease reveals changes associated with disease progression.Movement disorders : official journal of the Movement Disorder Society · 2015Article
- Somatic expression of unc-54 and vha-6 mRNAs declines but not pan-neuronal rgef-1 and unc-119 expression in aging Caenorhabditis elegans.Scientific reports · 2015Article
- High Protein Diet and Huntington's Disease.PloS one · 2015Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by a CAG trinucleotide expansion in the Huntingtin (Htt) gene. When the number of CAG repeats exceeds 36, the translated polyglutamine-expanded Htt protein interferes with the normal functions of many types of cellular machinery and causes cytotoxicity. Clinical symptoms include progressive involuntary movement disorders, psychiatric signs, cognitive decline, dementia, and a shortened lifespan. The most severe brain atrophy is observed in the striatum and cortex. Besides the well-characterized neuronal defects, recent studies showed that the functions of mitochondria and several key players in energy homeostasis are abnormally regulated during HD progression. Energy dysregulation thus is now recognized as an important pathogenic pathway of HD. This review focuses on the importance of three key molecular determinants (peroxisome proliferator-activated receptor-γ coactivator-1α, AMP-activated protein kinase, and creatine kinase B) of cellular energy homeostasis and their possible involvement in HD pathogenesis.
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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.