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Parent-of-origin Effect in Schizophrenia and Non-affective Psychoses: Evidence from Dermatoglyphics

OBJECTIVE: This study aims at examining “parent-of-origin effect” (POE) in dermatoglyphic patterns among patients with schizophrenia and non-affective psychoses. MATERIALS AND METHODS: Dermatoglyphic comparison was carried out for schizophrenia patients (n=200) and healthy controls (HC) (n=100). In...

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Detalles Bibliográficos
Autores principales: Divakaran, Anjith, Narayanaswamy, Janardhanan C., Kalmadi, Sunil V., Narayan, Vidya, Rao, Naren P., Venkatasubramanian, Ganesan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821203/
https://www.ncbi.nlm.nih.gov/pubmed/24249928
http://dx.doi.org/10.4103/0253-7176.119481
Descripción
Sumario:OBJECTIVE: This study aims at examining “parent-of-origin effect” (POE) in dermatoglyphic patterns among patients with schizophrenia and non-affective psychoses. MATERIALS AND METHODS: Dermatoglyphic comparison was carried out for schizophrenia patients (n=200) and healthy controls (HC) (n=100). In addition, the effect of family history and POE was examined in the dermatoglyphic pattern. RESULTS: Schizophrenia patients compared to HC had significantly lower left total finger ridge count (LTFRC) (t=3.63, P<0.001), right total finger ridge count (RTFRC) (t=4.86, P<0.001), and absolute finger ridge count (ATFRC) (t=4.80, P<0.001) compared to HC. It was also noted that patient group had significantly higher average number of arches (t=2.20, P=0.03). The comparison between the same sex POE group and the opposite sex POE group revealed that significant differences exist in LTFRC (t=2.91, P<0.01) and ATFRC (t=2.30, P=0.02). The same sex group also had lesser number of whorls compared to opposite sex group (t=2.04, P=0.04). CONCLUSIONS: The same sex parental inheritance group seem to be more developmentally compromised than the opposite sex parental inheritance group indicating a significant POE. Complex epigenetic mechanisms along with hormonal modulation could explain the sex specific disease phenotype expression, which is a plausible explanation as in the present study.