From Prader–Willi Syndrome to Psychosis: Translating Parent-of-Origin Effects into Schizophrenia Research

Abstract

Prader-Willi syndrome (PWS) is a relatively rare disorder that originates from paternally inherited deletions and maternal disomy (mUPD) within the 15q11-q13 region or alterations in the PWS imprinting center. Evidence is accumulating that mUPD underlies high prevalence of psychosis among PWS patients. Several genes involved in differentiation and survival of neurons as well as neurotransmission known to act in the development of PWS have been also implicated in schizophrenia. In this article, we provide an overview of genetic and epigenetic underpinnings of psychosis in PWS indicating overlapping points in the molecular background of PWS and schizophrenia. Simultaneously, we highlight the need for studies investigating genetic and epigenetic makeup of the 15q11-q13 in schizophrenia indicating promising candidate genes.

Keywords::

• genomic imprinting
• parent-of-origin effects
• Prader–Willi syndrome
• psychosis
• schizophrenia

Financial & competing interests disclosure

B Misiak was supported by the START scholarship provided by the Foundation of Polish Science. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

B Misiak was supported by the START scholarship provided by the Foundation of Polish Science. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.