Thyroid Function in Causal Relation to MRI Markers of Cerebral Small Vessel Disease: A Mendelian Randomization Analysis
Authors' conclusion
This study indicated that genetically predicted increased TSH was associated with increased MD, as well as increased FT4 with increased FA, implying the causal effect of thyroid dysfunction on white matter microstructural injury. There were no significant causal relationships of hypothyroidism or hyperthyroidism with CSVD. Further investigations should verify these findings and clarify the underlying pathophysiological mechanisms.
Study context
- Population
- GWAS summary data: TSH, free thyroxine (FT4), hypothyroidism and hyperthyroidism; White matter hyperintensity (WMH), mean diffusivity, fractional anisotropyTSH 54,288 · FT4 49,269 · hyperthyroidism 51,823 · WMH 42,310 · mean diffusivity 17,467 · fractional anisotropy 17,663
- Comparison
- Genetically predicted TSH, FT4, hypothyroidism and hyperthyroidism vs MRI markers of cerebral small vessel disease (CSVD) (WMH, MD, fractional anisotropy (FA))
- Outcome
- Causal effects of genetically predicted thyroid function on 3 neuroimaging markers of CSVD (WMH, mean diffusivity, fractional anisotropy), inverse variance-weighted MR
Methodological detailsgenome-wide association variants, inverse variance-weighted primary analysis, sensitivity analyses: MR-PRESSO, MR-Egger, weighted median, weighted mode
- Genome-wide association variants
- Inverse variance-weighted primary analysis
- Sensitivity analyses: MR-PRESSO, MR-Egger, weighted median, weighted mode
Main finding
As reported in the abstract
Genetically increased TSH and mean diffusivity: β (95% CI 0.0763, 0.548; P = .01)
.311
Genetically increased FT4 and fractional anisotropy: β (95% CI 0.222, 0.858; P < .001)
.540
Further findings
Sensitivity analyses (different Mendelian randomization (MR) methods)
- Similar directions but lower precision
Original publication
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