ReviewBrain pathology (Zurich, Switzerland)1997
Toward understanding the molecular pathology of Huntington's disease.
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 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 72 citations in OpenAlex.
- Role of aging‑related cytokines in neurodegenerative disease (Review).International journal of molecular medicine · 2026Review
- RETRACTED: Neuroinflammatory Markers: Key Indicators in the Pathology of Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2022Review
- Endogenous mouse huntingtin is highly abundant in cranial nerve nuclei, co-aggregates to Abeta plaques and is induced in reactive astrocytes in a transgenic mouse model of Alzheimer's disease.Acta neuropathologica communications · 2019Article
- An in vitro perspective on the molecular mechanisms underlying mutant huntingtin protein toxicity.Cell death & disease · 2012Review
- Article
- Neuroprotection for Huntington's disease: ready, set, slow.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2008Review
- Imaging in cell-based therapy for neurodegenerative diseases.European journal of nuclear medicine and molecular imaging · 2005Review
- Firing up the nature/nurture controversy: bioethics and genetic determinism.Journal of medical ethics · 2005Article
- Using advances in neuroimaging to detect, understand, and monitor disease progression in Huntington's disease.NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics · 2004Review
- Paternal factors and schizophrenia risk: de novo mutations and imprinting.Schizophrenia bulletin · 2001Review
- An actin-binding protein of the Sla2/Huntingtin interacting protein 1 family is a novel component of clathrin-coated pits and vesicles.The Journal of cell biology · 1999Article
- The cellular and subcellular localization of huntingtin-associated protein 1 (HAP1): comparison with huntingtin in rat and human.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's Disease (HD) is caused by expansion of a CAG trinucleotide beyond 35 repeats within the coding region of a novel gene. Recently, new insights into the relationship between CAG expansion in the HD gene and pathological mechanisms have emerged. Survival analysis of a large cohort of affected and at-risk individuals with CAG sizes between 39 and 50 repeats have yielded probability curves of developing HD symptoms and dying of HD by a certain age. Animals transgenic for the first exon of huntingtin with large CAG repeats lengths have been reported to have a complex neurological phenotype that bears interesting similarities and differences to HD. The repertoire of huntingtin-interacting proteins continues to expand with the identification of HIP1, a protein whose yeast homologues have known functions in regulating events associated with the cytoskeleton. The ability of huntingtin to interact with two of its four known protein partners appears to be influenced by CAG length. Caspase 3 (apopain), a key cysteine protease known to play a seminal role in neural apoptosis, has also been demonstrated to specifically cleave huntingtin in a CAG length-dependent manner. Many of these features are combined in a model suggesting mechanisms by which the pathogenesis of HD may be initiated. The development of appropriate in vitro and animal models for HD will allow the validity of these models to be tested.
Indexed as
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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.