Evidence mapPaperPMID 39820855Full record

ReviewNeurogenetics2025

Neuroinflammation and neurodegeneration in Huntington's disease: genetic hallmarks, role of metals and organophosphates.

Omkar Kumar Kunwar, Shamsher Singh

Abstract readReview
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Omkar Kumar KunwarNeuropharmacology Division, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India.
Shamsher SinghNeuropharmacology Division, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, 142001, India. shamshersinghbajwa@gmail.com.ORCID https://orcid.org/0000-0002-2780-6632

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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

Huntington DiseaseMetalsNeuroinflammatory DiseasesOrganophosphatesAnimalsHumansHuntingtin ProteinHuntingtin ProteinMetalsOrganophosphatesChlorpyrifosDopamine dysfunctionExcitotoxicityHuntington’s diseaseNeuroinflammation

Identifiers

PMID39820855

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.