Exploring the Role of Plasma Lipids and Statins Interventions on Multiple Sclerosis Risk and Severity: A Mendelian Randomization Study Article Swipe
Mona M. Almramhi
,
Chris Finan
,
Catherine S. Storm
,
Amand F. Schmidt
,
Demis A. Kia
,
Rachel Coneys
,
Sandesh Chopade
,
Aroon D. Hingorani
,
Nicholas Wood
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1101/2022.08.01.22277781
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1101/2022.08.01.22277781
Background There has been considerable interest in statins due to their pleiotropic effects beyond their lipid-lowering properties. Many of these pleiotropic effects are predominantly ascribed to their capacity to inhibit the isoprenylation of Rho small guanosine triphosphatases (Rho GTPases). We aimed to genetically investigate the role of lipids and statin interventions on multiple sclerosis (MS) risk and severity. Method We employed two-sample Mendelian randomization (MR) to: (1) investigate the causal role of lipids (high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG)) levels in MS risk and severity, (2) genetically mimic both cholesterol-dependent (via low-density lipoprotein cholesterol (LDL-C) and cholesterol biosynthesis pathway) and cholesterol-independent (via Rho GTPases) effects of statins on MS risk and MS severity. Results The results of MR using the inverse variance weighted method show that lifelong higher HDL-C (OR 1.14 (95% CI 1.04 to1.26), p-value 7.94E-03) increase MS risk, but LDL-C and TG were not. MR results also show that genetically predicted RAC2 (OR 0.86 (95% CI 0.78 to 0.95), p-value 3.80E-03) is implicated causally in reducing MS risk. Furthermore, we found no evidence for the causal role of lipids and genetically mimicked statins on MS severity. There is no evidence of reverse causation between MS risk and lipids. Conclusions Evidence from this study suggests that HDL-C is a risk factor for MS development. The MR findings suggest that RAC2 (a member of Rho GTPases) is a potent genetic modifier of MS risk. Since RAC2 has been reported to mediate some of the pleiotropic effects of statins, we suggest that statins reduce MS risk via a RAC2 -related mechanism(s) (i.e., cholesterol-independent pathway).
Related Topics
Concepts
Mendelian randomization
Internal medicine
Cholesterol
GTPase
Endocrinology
Lipoprotein
Medicine
Biology
Genetics
Gene
Genetic variants
Genotype
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2022.08.01.22277781
- https://www.medrxiv.org/content/medrxiv/early/2022/08/05/2022.08.01.22277781.full.pdf
- OA Status
- green
- Cited By
- 2
- References
- 44
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4290039830
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4290039830Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1101/2022.08.01.22277781Digital Object Identifier
- Title
-
Exploring the Role of Plasma Lipids and Statins Interventions on Multiple Sclerosis Risk and Severity: A Mendelian Randomization StudyWork title
- Type
-
preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2022Year of publication
- Publication date
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2022-08-05Full publication date if available
- Authors
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Mona M. Almramhi, Chris Finan, Catherine S. Storm, Amand F. Schmidt, Demis A. Kia, Rachel Coneys, Sandesh Chopade, Aroon D. Hingorani, Nicholas WoodList of authors in order
- Landing page
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https://doi.org/10.1101/2022.08.01.22277781Publisher landing page
- PDF URL
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https://www.medrxiv.org/content/medrxiv/early/2022/08/05/2022.08.01.22277781.full.pdfDirect link to full text PDF
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YesWhether a free full text is available
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-
greenOpen access status per OpenAlex
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https://www.medrxiv.org/content/medrxiv/early/2022/08/05/2022.08.01.22277781.full.pdfDirect OA link when available
- Concepts
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Mendelian randomization, Internal medicine, Cholesterol, GTPase, Endocrinology, Lipoprotein, Medicine, Biology, Genetics, Gene, Genetic variants, GenotypeTop concepts (fields/topics) attached by OpenAlex
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2Total citation count in OpenAlex
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2023: 1, 2022: 1Per-year citation counts (last 5 years)
- References (count)
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44Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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