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Related Experiment Videos

Gene-Environment Interactions in Multiple Sclerosis: A UK Biobank Study.

Benjamin Meir Jacobs1, Alastair J Noyce1, Jonathan Bestwick1

  • 1From the Preventive Neurology Unit, Wolfson Institute of Preventive Medicine, Barts and Queen Mary University of London; and Royal London Hospital, Barts Health NHS Trust.

Neurology(R) Neuroimmunology & Neuroinflammation
|May 29, 2021
PubMed
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Genetic risk significantly interacts with childhood obesity in multiple sclerosis (MS) development. This finding highlights the importance of considering both genetic predisposition and environmental factors like obesity for MS prevention strategies.

Area of Science:

  • Neuroimmunology
  • Genetic Epidemiology
  • Environmental Health

Background:

  • Multiple sclerosis (MS) etiology involves complex interactions between genetic susceptibility and environmental risk factors.
  • Understanding these interactions is crucial for developing effective prevention and treatment strategies for MS.
  • Polygenic risk scores (PRS) offer a tool to quantify an individual's genetic predisposition to MS.

Purpose of the Study:

  • To investigate the potential interaction between genetic risk, quantified by PRS, and environmental risk factors for MS.
  • To determine if genetic predisposition modifies the impact of environmental exposures on MS risk.
  • To identify specific environmental factors that interact with genetic risk in the context of MS.

Main Methods:

  • Utilized UK Biobank data, identifying MS cases through ICD-10 codes and self-report.

Related Experiment Videos

  • Calculated PRS, both including (PRS_MHC) and excluding (PRS_non-MHC) the Major Histocompatibility Complex region.
  • Employed multivariable logistic regression and interaction analyses (attributable proportion due to interaction - AP) to assess the interplay between genetic and environmental factors.

    • Main Results:

    • Childhood obesity, early menarche, and smoking were confirmed as MS risk factors.
    • PRS demonstrated strong association with MS risk in the validation cohort.
    • Significant interaction was observed between polygenic risk for MS and childhood obesity (AP = 0.17 for both PRS_MHC and PRS_non-MHC).

    Conclusions:

    • This study provides novel evidence for a significant interaction between genetic risk burden and childhood obesity in the development of MS.
    • These findings underscore the importance of addressing childhood obesity as a modifiable risk factor in individuals with high genetic susceptibility to MS.
    • The results have implications for understanding MS pathogenesis and for designing targeted public health interventions and personalized prevention strategies.