ArticleFrontiers in neuroanatomy2011
Huntington's Disease and Striatal Signaling.
Article in Frontiers in neuroanatomy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Hypertension, antihypertensive drugs, and age at onset of Huntington's disease.Orphanet journal of rare diseases · 2023Pooled it
- Trial
- c-Jun in neurodegeneration: A key transcriptional regulator with therapeutic implications.Molecular therapy. Nucleic acids · 2026Review
- A Two-Track Model of Huntington's Disease Pathology: Striatal Atrophy Mediates Maladaptive Immune Dysregulation.International journal of molecular sciences · 2026Article
- Pridopidine, a Potent and Selective Therapeutic Sigma-1 Receptor (S1R) Agonist for Treating Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mild cognitive impairment in Huntington's disease: challenges and outlooks.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- The Dynamics of Dopamine DNeuroscience bulletin · 2023Article
- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- Altered Cholesterol Homeostasis in Huntington's Disease.Frontiers in aging neuroscience · 2022Review
- Review
- Accelerated expansion of pathogenic mitochondrial DNA heteroplasmies in Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Structural Insights into Ankyrin Repeat-Containing Proteins and Their Influence in Ubiquitylation.International journal of molecular sciences · 2021Review
- Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Protects Striatal Cells and Improves Motor Function in Huntington's Disease Models: Role of PAC1 Receptor.Frontiers in pharmacology · 2021Article
- FACS-array-based cell purification yields a specific transcriptome of striatal medium spiny neurons in a murine Huntington disease model.The Journal of biological chemistry · 2020Article
- Proteomic Analysis of the Spinophilin Interactome in Rodent Striatum Following Psychostimulant Sensitization.Proteomes · 2018Article
- Sex-dependent behavioral impairments in the HdhQ350/+ mouse line.Behavioural brain research · 2018Article
- PERK-opathies: An Endoplasmic Reticulum Stress Mechanism Underlying Neurodegeneration.Current Alzheimer research · 2016Review
- Impaired TrkB Signaling Underlies Reduced BDNF-Mediated Trophic Support of Striatal Neurons in the R6/2 Mouse Model of Huntington's Disease.Frontiers in cellular neuroscience · 2016Article
- Evaluating the SERCA2 and VEGF mRNAs as Potential Molecular Biomarkers of the Onset and Progression in Huntington's Disease.PloS one · 2015Article
- ER stress-induced eIF2-alpha phosphorylation underlies sensitivity of striatal neurons to pathogenic huntingtin.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's Disease (HD) is the most frequent neurodegenerative disease caused by an expansion of polyglutamines (CAG). The main clinical manifestations of HD are chorea, cognitive impairment, and psychiatric disorders. The transmission of HD is autosomal dominant with a complete penetrance. HD has a single genetic cause, a well-defined neuropathology, and informative pre-manifest genetic testing of the disease is available. Striatal atrophy begins as early as 15 years before disease onset and continues throughout the period of manifest illness. Therefore, patients could theoretically benefit from therapy at early stages of the disease. One important characteristic of HD is the striatal vulnerability to neurodegeneration, despite similar expression of the protein in other brain areas. Aggregation of the mutated Huntingtin (HTT), impaired axonal transport, excitotoxicity, transcriptional dysregulation as well as mitochondrial dysfunction, and energy deficits, are all part of the cellular events that underlie neuronal dysfunction and striatal death. Among these non-exclusive mechanisms, an alteration of striatal signaling is thought to orchestrate the downstream events involved in the cascade of striatal dysfunction.
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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.