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A Strategy to Identify de Novo Mutations in Common Disorders such as Autism and Schizophrenia

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Published on: June 15, 2011

PRODH variants and risk for schizophrenia.

Alecia Willis¹, Hans Uli Bender, Gary Steel

¹McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

|June 6, 2008

Summary

Genetic variants in PRODH, an enzyme in proline metabolism, may increase schizophrenia risk. This review critically examines evidence, suggesting further research into proline

Area of Science:

Neuropsychiatric Disorders
Human Genetics
Biochemical Pathways

Background:

Schizophrenia is a prevalent neuropsychiatric disorder with an unknown cause.
Proline and its catabolism enzyme, PRODH, are implicated in schizophrenia risk.
Existing research presents conflicting findings regarding PRODH's role.

Purpose of the Study:

To critically review existing data on proline metabolism and schizophrenia risk.
To evaluate the evidence supporting PRODH variants in schizophrenia etiology.
To propose future research directions.

Main Methods:

Literature review of human and model organism studies.
Analysis of proline metabolism pathways.
Critical assessment of genetic association data.

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Main Results:

Conflicting study results highlight the complexity of PRODH's role.
Evidence suggests certain loss-of-function PRODH variants confer risk.
Proline metabolism is a significant area for schizophrenia research.

Conclusions:

Loss-of-function PRODH variants are associated with schizophrenia risk in some individuals.
Further research is needed to elucidate the precise mechanisms.
Proline metabolism represents a potential therapeutic target.