ReviewNeurogenetics2025
Neuroinflammation and neurodegeneration in Huntington's disease: genetic hallmarks, role of metals and organophosphates.
Review in Neurogenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed.
- From glycemic control to neuroprotection: alogliptin as a repurposed candidate for Huntington's disease.Metabolic brain disease · 2026Review
- α-Klotho as a central integrative signalling hub in cognitive function and neuroprotection in neurodegenerative diseases.Metabolic brain disease · 2026Review
- Review
- Therapeutic potential of sulforaphane in neurodegenerative diseases: mechanistic Insights into Nrf2, NF-κB, TrkB, SIRT1, MAPK, and JAK/STAT signalling pathways.Molecular biology reports · 2026Review
- Role of Pentacyclic Triterpenes in the Management of Neurological Disorders: An Insight into Molecular Mechanisms and Therapeutic Approaches.Molecular neurobiology · 2026Review
- The interplay between inflammation and oxidative stress in depression: pathogenic mechanisms and treatment approaches.Molecular biology reports · 2025Review
- The KEAP1-Cullin3-RBX1-Nrf2 Axis in Redox Homeostasis: Molecular Mechanisms, Pathophysiological Roles, and Precision Therapeutic Opportunities.Molecular neurobiology · 2025Review
- Anti-inflammatory and antioxidant effects of baicalein: targeting Nrf2, and NFĸB in neurodegenerative disease.Inflammopharmacology · 2025Review
- Advances in Huntington's Disease Biomarkers: A 10-Year Bibliometric Analysis and a Comprehensive Review.Biology · 2025Review
- CRISPR-Cas technologies in neurodegenerative disorders: mechanistic insights, therapeutic potential, and translational challenges.Frontiers in neurology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HDs) is a fatal, autosomal dominant, and hereditary neurodegenerative disorder characterized by progressive motor dysfunction, cognitive decline, and psychiatric disturbances. HD is well linked to mutation in the HTT gene, which leads to an abnormal expansion of trinucleotide CAG repeats, resulting in the production of the mHTT protein and responsible for abnormally long poly-Q tract. These abnormal proteins disrupt cellular processes, including neuroinflammation, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction, ultimately leading to selective neuronal loss in the brain. Epidemiological studies reveal significant regional variability in HDs prevalence, with the highest rates observed in North America and the lowest in Africa. In addition to genetic factors, environmental influences such as exposure to metals, and chemicals, and lifestyle factors like alcohol and tobacco use may exacerbate disease progression. This review explores the molecular mechanisms underlying HDs and emphasize the role of neuroinflammatory mediators and environmental factors, in HD research. Understanding these complex interactions is crucial for developing targeted interventions that can slow or halt the progression of this devastating disease.
Indexed as
Identifiers
39820855What Socratic 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 Socratic graph.