EPV776 - Family-Based Study of Dermatoglyphic Patterns and Stress-Related Genetic Variability in Schizophrenia

EPV776

Family-Based Study of Dermatoglyphic Patterns and Stress-Related Genetic Variability in Schizophrenia

M. M. Moreira Martinez ^{1 2 3,*}, N. Hostalet ^{4 5 6}, A. Sotero-Moreno ^{4 5}, C. Almodóvar-Payá ^{4 5 6}, M. J. Muñoz ⁷, L. Fañanás ^{5 6}, S. Miret ^{5 8}, M. Giralt-López ^{1 2 3}, M. Fatjó-Vilas ^{4 5 6}

¹Child and Adolescent Psychiatry Department, Germans Trias i Pujol University Hospital, ²Germans Trias i Pujol Research Institute, Badalona, ³Department of Psychiatry and Legal Medicine, Autonomous University of Barcelona, Cerdanyola del Vallès, ⁴FIDMAG Germanes Hospitalàries Research Foundation, Barcelona, ⁵CIBERSAM ((Biomedical Research Network in Mental Health; Instituto de Salud Carlos III), Madrid, ⁶Department of Evolutionary Biology, Ecology and Environmental Sciences, Faculty of Biology, University of Barcelona, Barcelona, ⁷Adolescent Psychiatry Unit, Fundación Hospitalarias Sant Boi, Sant Boi de Llobregat, ⁸Adult Mental Health Centre, Psychiatry, Mental Health and Addictions Service, Santa Maria University Hospital, Lleida, Spain

 

Introduction: Schizophrenia Spectrum Disorders (SSD) are neurodevelopmental conditions shaped by genetic and environmental factors during early brain development. Dermatoglyphic patterns can serve as markers of early developmental disruptions, with features such as simplified fingerprints and greater asymmetry observed more frequently in SSD patients and, to a lesser extent, in their unaffected relatives. Stress-regulation systems, particularly the corticotropin-releasing hormone (CRH) and endocannabinoid (ECS) pathways, are also implicated in SSD risk, yet their potential associations with dermatoglyphic variations remain largely unexplored.

Objectives: To assess if variants in stress-related genes affect the transmission of dermatoglyphic traits in SSD.

Methods: We studied 61 families (n = 208), including SSD patients and their unaffected relatives. Hand and finger dermatoglyphic patterns were assessed. Seven SNPs from Corticotropin-releasing hormone receptor 1 gene (CRHR1) and Cannabinoid Receptors type 1 and 2 (CNR1, CNR2) were genotyped. Family-based associations were tested using quantitative transmission disequilibrium tests (QTDT analysis/Unphased).

Results: Genetic variants at CRHR1 (rs17689966 and rs171440) and CNR2 (rs2501431) were associated with the preferential transmission of higher finger and palmar asymmetric dermatoglyphic patterns from parents to affected offspring. The same pattern was detected for one CRHR1 haplotype (rs171440–rs17689966) in relation to palmar dermatoglyphic ridge counts. 

Conclusions: Dermatoglyphic asymmetry may serve as a non-invasive marker of developmental instability linked to variations in stress-regulation genes, reinforcing the role of combined genetic and prenatal stress risk in SSD.

Acknowledgements: ISCIII project-PI20/01002, grant-FI21/00093-NH, grant-CP20/00072-MFV, mobility grant-MV23/00059-NH, co-funded by ERDF/ESF; AGAUR: 2021SGR01475.

 

Disclosure of Interest: None Declared