ReviewBrain pathology (Zurich, Switzerland)2000
Toward an understanding of polyglutamine neurodegeneration.
Review in Brain pathology (Zurich, Switzerland), 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 57 citations in OpenAlex.
- Altered endoplasmic reticulum stress response in non-infectious neuronal cytoplasmic inclusions in the brain of an aged dog.Veterinary research communications · 2025Article
- Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration.ACS chemical neuroscience · 2024Review
- Diverse single-amino-acid repeat profiles in the genus Cryptosporidium.Parasitology · 2018Article
- Selection pressure on human STR loci and its relevance in repeat expansion disease.Molecular genetics and genomics : MGG · 2016Article
- Enhanced aggregation of androgen receptor in induced pluripotent stem cell-derived neurons from spinal and bulbar muscular atrophy.The Journal of biological chemistry · 2013Article
- RNAi: a potential new class of therapeutic for human genetic disease.Human genetics · 2011Review
- Synchrotron infrared microspectroscopy detecting the evolution of Huntington's disease neuropathology and suggesting unique correlates of dysfunction in white versus gray brain matter.Analytical chemistry · 2011Article
- Deciphering the structure, growth and assembly of amyloid-like fibrils using high-speed atomic force microscopy.PloS one · 2010Article
- Spinocerebellar ataxia type 3 (SCA3): thalamic neurodegeneration occurs independently from thalamic ataxin-3 immunopositive neuronal intranuclear inclusions.Brain pathology (Zurich, Switzerland) · 2006Article
- Spinocerebellar ataxias types 2 and 3: degeneration of the pre-cerebellar nuclei isolates the three phylogenetically defined regions of the cerebellum.Journal of neural transmission (Vienna, Austria : 1996) · 2005Article
- Lentiviral-mediated delivery of mutant huntingtin in the striatum of rats induces a selective neuropathology modulated by polyglutamine repeat size, huntingtin expression levels, and protein length.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- An expanded glutamine repeat destabilizes native ataxin-3 structure and mediates formation of parallel beta -fibrils.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Inflammatory genes are upregulated in expanded ataxin-3-expressing cell lines and spinocerebellar ataxia type 3 brains.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Introduction: Targeted modulation of neuronal apoptosis: a double-edged sword?Brain pathology (Zurich, Switzerland) · 2000Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyglutamine expansion is now recognized to be a major cause of inherited human neurodegenerative disease. The polyglutamine expansion diseases identified so far are slowly progressive disorders in which distinct yet overlapping brain regions are selectively vulnerable to degeneration. Despite their clinical differences these diseases likely share a common pathogenic mechanism, occurring at the protein level and centered on an abnormal conformation of expanded polyglutamine in the respective disease proteins. Recently there has been remarkable progress in our understanding of polyglutamine disease, but still there are many unanswered questions. In this review, I first outline some of the shared features of polyglutamine diseases and then discuss several issues relevant to an understanding of pathogenesis, paying particular attention to possible mechanisms of neurotoxicity.
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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.