Evidence map›Paper›PMID 39810445›Full record

ReviewEndocrine, metabolic & immune disorders drug targets2025

The Polygenic Nature of Multiple Sclerosis: Genetic Variants, Immunological Modulation, and Environmental Connections.

Zuber Khan, Sidharth Mehan, Pankaj Kumar Maurya, Aakash Kumar, Ghanshyam Das Gupta, Acharan S Narula, Reni Kalfin

Abstract readReview
In one paragraph

Review in Endocrine, metabolic & immune disorders drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Frontiers in pharmacology · 2025
    Review
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

7 authors.

Zuber KhanDivision of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India; Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, 144603, India.
Sidharth MehanDivision of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India; Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, 144603, India.
Pankaj Kumar MauryaDivision of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India; Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, 144603, India.
Aakash KumarDivision of Neuroscience, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India; Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, 144603, India.
Ghanshyam Das GuptaDepartment of Pharmaceutics, ISF College of Pharmacy, Moga, Punjab, India Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, 144603, India.
Acharan S NarulaNarula Research, LLC, 107 Boulder Bluff, Chapel Hill, NC27516, USA.
Reni KalfinInstitute of Neurobiology, Bulgarian Academy of Sciences, Acad. G. Bonchev St., Block 23, Sofia, 1113, Bulgaria.

Funding

Department of Science and Technology, Science and Engineering Board, DSTSERB, CRG (Core Research Grant) CRG/2021/001009
6 · The paper itself

Abstract

Multiple Sclerosis (MS), a debilitating inflammatory disorder of the central nervous system characterized by demyelination, is significantly influenced by polygenic variations. Although the precise cause of MS remains unclear, it is believed to arise from a complex interplay of genetic and environmental factors. Recent investigations have focused on the polygenic nature of genetic alterations linked to MS risk. This review highlights the critical role of these genetic variants in shaping disease susceptibility and progression. Specific Human Leukocyte Antigen (HLA) alleles, such as HLA-DRB1*15:01, HLA-DRB50*101, HLA-DR2+, HLA-DQ6, DQA 0102, and DQB1 0602, are implicated in immune modulation, significantly increasing the risk of developing MS. Additionally, Genome-wide Association Studies (GWAS) have identified non-HLA genetic variants that contribute to MS susceptibility, including IL-2RA (rs2104286), IL-7R (rs6897932), CD40 (rs1883832 T), CD58 (rs2300747), and others, each playing a role in immune regulation and disease progression. Dysfunctions in genes regulating myelin integrity, such as MOG (Myelin Oligodendrocyte Glycoprotein), MAG (Myelin-associated Glycoprotein), and PLP1 (Proteolipid Protein 1), further drive MS pathogenesis. Moreover, viral infections, notably Epstein-Barr Virus (EBV), Human Herpesvirus 6 (HHV-6), and measles virus, may exacerbate the development of MS by triggering immune responses. Understanding the contribution of these genetic and viral factors may shed light on the complex etiology of MS. Polygenic Risk Scores (PRS) provide a valuable tool for estimating MS susceptibility based on the cumulative effect of genetic variants. However, translating these genetic insights into clinical practice requires further validation, including environmental considerations. Investigating MS polygenicity could lead to personalized therapies, enhancing diagnosis, prognosis, and treatment, ultimately improving outcomes for MS patients.

Indexed as

Gene-Environment InteractionGenetic VariationMultifactorial InheritanceMultiple SclerosisAnimalsGenetic Predisposition to DiseaseGenome-Wide Association StudyHLA AntigensHumansHLA Antigensdemyelinationdiagnosis.genetic variantsgenome-wide association studyMultiple sclerosispolygenic risk score

Identifiers

PMID39810445
PMCPMC12481567

What Socratic holds

Textmetadata
LicenceCC BY
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.