• FluTrackers.com Inc. does not provide medical advice. Information on this web site is collected from various internet resources, and the FluTrackers board of directors makes no warranty to the safety, efficacy, correctness or completeness of the information posted on this site by any author or poster. The information collated here is for instructional and/or discussion purposes only and is NOT intended to diagnose or treat any disease, illness, or other medical condition. Every individual reader or poster should seek advice from their personal physician/healthcare practitioner before considering or using any interventions that are discussed on this website. By continuing to access this website you agree to consult your personal physican before using any interventions posted on this website, and you agree to hold harmless FluTrackers.com Inc., the board of directors, the members, and all authors and posters for any effects from use of any medication, supplement, vitamin or other substance, device, intervention, etc. mentioned in posts on this website, or other internet venues referenced in posts on this website.
  • We are not asking for any donations. Do not donate to any entity who says they are raising funds for us.

Sci Rep . Brain structures as potential mediators of the causal effect of COVID 19 on migraine risk

tetano

Editor, Senior Moderator
Sci Rep


. 2024 Nov 13;14(1):27895.
doi: 10.1038/s41598-024-79530-9. Brain structures as potential mediators of the causal effect of COVID 19 on migraine risk

Hongbei Xu[SUP] #[/SUP][SUP] 1 [/SUP], Wei Chen[SUP] #[/SUP][SUP] 2 [/SUP], Yaxin Ju[SUP] 3 [/SUP], Hongqun Chen[SUP] 2 [/SUP], Ping Yuan[SUP] 2 [/SUP], Fu Ouyang[SUP] 4 [/SUP]



Affiliations
Abstract

Migraine is a common neurological disorder observed after coronavirus disease 2019 (COVID 19) infection. However, the intricate relationship between COVID 19 and migraine, particularly the potential mediating role of brain imaging-derived phenotypes (BIPs), remains unclear. This study used linkage disequilibrium score regression (LDSC), a bidirectional two-sample Mendelian randomization (MR) approach, and two-step MR analysis to investigate potential causal links. The robustness of the MR findings was corroborated through generalized summary-data-based Mendelian randomization (GSMR) and MR-Steiger methods. The results of the LDSC analysis revealed that the genetic correlation coefficient between COVID 19 traits and migraine was 0.0277 for infection (P = 0.0051), 0.1690 for hospitalization (P = 0.0016), and 0.1147 for severity (P = 0.0330). The genetic correlation coefficients between COVID 19 infection, hospitalization, severity and migraine and migraine with aura (MA) were 0.2654 (P = 0.0012), 0.2065 (P = 0.0043), and 0.1537 (P = 0.0230), respectively. Two-sample MR analysis revealed a significant causal association of COVID 19 infection (odds ratio [OR] 1.2502, P = 0.0083; OR 1.4956, P = 0.0084), hospitalization (OR 1.0689, P = 0.0138; OR 1.0919, P = 0.0208), and severity (OR 1.0644, P = 0.0072; OR 1.0844, P = 0.0098) with increased risk of migraine and migraine with aura (MA). Cortical thickness (CT), total surface area (TSA), and fractional anisotropy (FA) were identified as BIP intermediaries in the risk trajectory from COVID 19 to migraine. The TSA exhibited a more pronounced mediating effect than did CT. This study revealed that genetically predicted COVID 19 is associated with an increased risk of migraine and MA, and BIPs act as potential mediators of these causal relationships, offering insights into the neurobiological underpinnings of migraine in the context of COVID 19.


 
Back
Top Bottom