ReviewNeuroscience2011
Pathophysiology of Huntington's disease: time-dependent alterations in synaptic and receptor function.
Review in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 2 of them syntheses that pooled it.
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
169 citing papers in PubMed, 2 syntheses or guidelines pooled it, 319 citations in OpenAlex.
- [European journal of nuclear medicine and molecular imaging · 2023Pooled it
- Therapeutic Use of Music, Dance, and Rhythmic Auditory Cueing for Patients with Huntington's Disease: A Systematic Review.Journal of Huntington's disease · 2019Pooled it
- Review
- Molecular Mechanisms of Neurodegenerative Diseases: Emerging Biomarkers and Therapeutic Targets.Brain sciences · 2026Review
- An Open-Label Phase 1b Study of the Safety, Pharmacokinetics, Pharmacodynamics, and Clinical Activity of ANX005 in Patients with Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Article
- Synaptic aging and neurodegeneration: the role of synaptic vesicle dynamics and neurotransmitter imbalance.Biogerontology · 2026Review
- Fingolimod Effects on Motor Function and BDNF-TrkB Signaling in a Huntington's Mouse Model Are Disease-Stage-Dependent.International journal of molecular sciences · 2026Article
- Review
- Restoring endogenous Dlg4/PSD95 expression by an artificial transcription factor ameliorates cognitive and motor learning deficits in the R6/2 mouse model of Huntington's disease.Clinical epigenetics · 2025Article
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- Upregulation of endocannabinoid signaling in vivo restores striatal synaptic plasticity and motor performance in Huntington's disease mice.Journal of Huntington's disease · 2025Article
- Presymptomatic targeted circuit manipulation for ameliorating Huntington's disease pathogenesis.iScience · 2025Article
- NMDA receptors in neurodegenerative diseases: mechanisms and emerging therapeutic strategies.Frontiers in aging neuroscience · 2025Review
- Engineered AAV capsid transport mutants overcome transduction deficiencies in the aged CNS.Molecular therapy. Nucleic acids · 2024Article
- Review
- Presymptomatic Targeted Circuit Manipulation for Ameliorating Huntington's Disease Pathogenesis.bioRxiv : the preprint server for biology · 2024Article
- Age- and region-dependent cortical excitability in the zQ175 Huntington disease mouse model.Human molecular genetics · 2024Article
- Neurodegenerative Diseases: New Hopes and Perspectives.Current molecular medicine · 2024Review
- Microglia and complement mediate early corticostriatal synapse loss and cognitive dysfunction in Huntington's disease.Nature medicine · 2023Article
109 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is a progressive, fatal neurological condition caused by an expansion of CAG (glutamine) repeats in the coding region of the Huntington gene. To date, there is no cure but great strides have been made to understand pathophysiological mechanisms. In particular, genetic animal models of HD have been instrumental in elucidating the progression of behavioral and physiological alterations, which had not been possible using classic neurotoxin models. Our groups have pioneered the use of transgenic HD mice to examine the excitotoxicity hypothesis of striatal neuronal dysfunction and degeneration, as well as alterations in excitation and inhibition in striatum and cerebral cortex. In this review, we focus on synaptic and receptor alterations of striatal medium-sized spiny (MSNs) and cortical pyramidal neurons in genetic HD mouse models. We demonstrate a complex series of alterations that are region-specific and time-dependent. In particular, many changes are bidirectional depending on the degree of disease progression, that is, early vs. late, and also on the region examined. Early synaptic dysfunction is manifested by dysregulated glutamate release in striatum followed by progressive disconnection between cortex and striatum. The differential effects of altered glutamate release on MSNs originating the direct and indirect pathways is also elucidated, with the unexpected finding that cells of the direct striatal pathway are involved early in the course of the disease. In addition, we review evidence for early N-methyl-D-aspartate receptor (NMDAR) dysfunction leading to enhanced sensitivity of extrasynaptic receptors and a critical role of GluN2B subunits. Some of the alterations in late HD could be compensatory mechanisms designed to cope with early synaptic and receptor dysfunctions. The main findings indicate that HD treatments need to be designed according to the stage of disease progression and should consider regional differences.
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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.