PPARD May Play a Protective Role against the Development of Schizophrenia
PPARD has been suggested to contribute to the etiology of schizophrenia (SCZ) with the underlying mechanisms largely unknown. Here, we first collected and analyzed the PPARD expression profile from three groups: (1) 18 healthy control (HC) subjects, (2) 14 clinical high-risk (CHR) patients, and (3)...
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Published in | PPAR research Vol. 2020; no. 2020; pp. 1 - 6 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Publishing Corporation
2020
Hindawi John Wiley & Sons, Inc Wiley |
Subjects | |
Online Access | Get full text |
ISSN | 1687-4757 1687-4765 |
DOI | 10.1155/2020/3480412 |
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Summary: | PPARD has been suggested to contribute to the etiology of schizophrenia (SCZ) with the underlying mechanisms largely unknown. Here, we first collected and analyzed the PPARD expression profile from three groups: (1) 18 healthy control (HC) subjects, (2) 14 clinical high-risk (CHR) patients, and (3) 19 early onset of SCZ (EOS) patients. After that, we conducted a systematical pathway analysis to explore the potential mechanisms involved in PPARD exerting influence on the pathological development of SCZ. Compared to the HC group, the expression of PPARD was slightly decreased in the EOS group (LFC=−0.34; p=0.23) and increased in the CHR group (LFC=0.65; p=0.20). However, there was a significant difference between the EOS group and the CHR group (LFC=−0.99; p=0.015), reflecting the amount of variation in PPARD expression before and after the onset of SCZ. Pathway analysis suggested that overexpression of PPARD may regulate ten proteins or molecules to inhibit the pathological development of SCZ, including the deactivation of eight SCZ promoters and stimulation of two SCZ inhibitors. Our results support the association between PPARD and SCZ. The pathways identified may help in the understanding of the potential mechanisms by which PPARD contributes to the etiology of SCZ. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Guest Editor: Anastasia Nesterova |
ISSN: | 1687-4757 1687-4765 |
DOI: | 10.1155/2020/3480412 |