ReviewBrain pathology (Zurich, Switzerland)1997
Clinical aspects of CAG repeat diseases.
Review in Brain pathology (Zurich, Switzerland), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 86 citations in OpenAlex.
- Protective effects of diacerein against quinolinic acid-induced Huntington's disease-like symptoms in adult zebrafish by targeting GSK-3β signalling.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Neuroinflammation and neurodegeneration in Huntington's disease: genetic hallmarks, role of metals and organophosphates.Neurogenetics · 2025Review
- NMR structures and magnetic force spectroscopy studies of small molecules binding to models of an RNA CAG repeat expansion.bioRxiv : the preprint server for biology · 2024Article
- Pathogenic mechanisms underlying spinocerebellar ataxia type 1.Cellular and molecular life sciences : CMLS · 2020Review
- The Role of Sex and Sex Hormones in Neurodegenerative Diseases.Endocrine reviews · 2020Review
- Main path and byways: non-vesicular glutamate release by system xc(-) as an important modifier of glutamatergic neurotransmission.Journal of neurochemistry · 2015Review
- Glutamine and Asparagine Side Chain Hyperconjugation-Induced Structurally Sensitive Vibrations.The journal of physical chemistry. B · 2015Article
- Chronic Glutamate Toxicity in Neurodegenerative Diseases-What is the Evidence?Frontiers in neuroscience · 2015Review
- Androgen receptor gene mutation, rearrangement, polymorphism.Translational andrology and urology · 2013Article
- PGC-1α rescues Huntington's disease proteotoxicity by preventing oxidative stress and promoting TFEB function.Science translational medicine · 2012Article
- Antioxidants in Huntington's disease.Biochimica et biophysica acta · 2012Review
- PGC-1α at the intersection of bioenergetics regulation and neuron function: from Huntington's disease to Parkinson's disease and beyond.Progress in neurobiology · 2012Review
- Effects of mutant huntingtin on mGluR5-mediated dual signaling pathways: implications for therapeutic interventions.Cellular and molecular neurobiology · 2010Article
- Role of glutamine deamidation in neurodegenerative diseases associated with triplet repeat expansions: a hypothesis.Journal of molecular neuroscience : MN · 2006Article
- Review
- COPASAAR--a database for proteomic analysis of single amino acid repeats.BMC bioinformatics · 2005Article
- Spinocerebellar degenerations: an update.Current neurology and neuroscience reports · 2002Review
- Huntington's Disease.Current treatment options in neurology · 2000Article
- Polyglutamine pathogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 1999Review
- Generation of neuronal intranuclear inclusions by polyglutamine-GFP: analysis of inclusion clearance and toxicity as a function of polyglutamine length.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
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
No grant is acknowledged in the PubMed record.
Abstract
Seven neurodegenerative disorders are known to be caused by unstable expansions of the trinucleotide CAG within human genes, and more will be discovered in the coming years. These disorders share some clinical similarities, as well as some differences, which are summarized here. These diseases have unusual clinical genetic properties related to the dynamic nature of CAG repeat expansions, including instability of the repeat expansion in meiosis, particularly male meiosis; a strong correlation between onset age and size of the repeat expansion; anticipation (earlier disease onset in succeeding generations); new mutations arising from unstable, mutable alleles with a high-normal CAG repeat number; and reduced penetrance for alleles in the low-affected range. Much more remains to be learned about the molecular biology and clinical pathophysiology of this new class of genetic diseases.
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What OpenQuestion holds
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.