Structural insights into cortical morphometry and erectile dysfunction: a Mendelian randomization and genetic correlation study
Previous studies have disclosed that abnormal brain dynamics are involved in erectile dysfunction (ED). However, the association of cortical morphometry with ED remains unclear. To investigate the association of the surface area and thickness of the total cerebral cortex and 34 regions with ED, t...
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          | Main Authors: | , , , , | 
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| Format: | Article | 
| Language: | English | 
| Published: | MRE Press
    
        2024-11-01 | 
| Series: | Journal of Men's Health | 
| Subjects: | |
| Online Access: | https://oss.jomh.org/files/article/20230928-100/pdf/JOMH2024051105.pdf | 
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| Summary: | Previous studies have disclosed that abnormal brain dynamics are involved in 
erectile dysfunction (ED). However, the association of cortical morphometry with 
ED remains unclear. To investigate the association of the surface area and 
thickness of the total cerebral cortex and 34 regions with ED, this Mendelian 
Randomization (MR) study was performed. Summary statistics of the surface area 
and thickness of cerebral cortex and ED were retrieved from previous genome-wide 
association studies. Genetic correlations between cortical morphometry and ED 
were evaluated by high-definition likelihood and linkage disequilibrium score 
regression (LDSC). Causal inference was made by the inverse variance weighting 
(IVW) estimator, supplemented by the MR-Egger, Weighted median, 
Maximum likelihood, MR. robust adjusted profile score, and MR-Pleiotropy Residual 
Sum and Outlier methods. The effect size of the surface area was scaled according 
to the standard deviation (SD). For surface area, the IVW estimator showed that a 
one SD increase of the entorhinal cortex and superior frontal cortex corresponded 
to a 1.25-fold (95% confidence interval (CI) = 1.03–1.53, p = 0.026) 
and a 1.24-fold (95% CI = 1.02–1.50, p = 0.031) risk of ED, 
respectively. LDSC regression found a significant genetic correlation between the 
surface area of the entorhinal cortex and ED (rg = 0.093, p < 
0.05). For thickness, the IVW method revealed that genetically proxied one 
millimeter increase of the inferior temporal cortex and paracentral cortex led to 
a 6.58-fold (95% CI = 1.16–37.14, p = 0.033) and a 7.99-fold (95% CI 
= 1.17–54.49, p = 0.034) risk of ED, respectively. The other five 
methods also supported these findings. No heterogeneity or pleiotropy was 
detected in the instrumental variables. This study supports that genetically 
proxied cortical morphometry is associated with an elevated risk of ED. This 
study provides new insights into the etiology of ED. | 
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| ISSN: | 1875-6867 1875-6859 | 
 
       