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Peripheral inflammation levels associated with degree of advanced brain aging in schizophrenia

Bibliographic Data

ID15516369
AuthorsFederica Klaus (0000-0002-7197-0632, University of California San Diego, corresponding author), Tanya T Nguyen (0000-0002-9510-9564, VA San Diego Healthcare System), Michael L Thomas (0000-0002-6896-272X, Colorado State University), Sharon C Liou (0000-0003-2769-3532, University of California San Diego), Benchawanna Soontornniyomkij (University of California San Diego), Kyle R Mitchell (0000-0001-5433-9569, VA San Diego Healthcare System), Rebecca Daly (0000-0001-6352-9188, Institute on Aging), Ashley Sutherland (0009-0005-0734-1769, University of California San Diego), Dilip V Jeste (0000-0002-1161-7351, Institute on Aging), Lisa T Eyler (0000-0002-7783-8798, University of California San Diego)
Year2022
Volume13
Pages966439-966439
Publication date2022-08-12
Open AccessYes
TypeARTICLE
VenueFrontiers in Psychiatry (JOURNAL)
Journal identifiersISSN: 1664-0640 • E-ISSN: 1664-0640
PublisherFrontiers Media (PUBLISHER • CH)
DOI10.3389/fpsyt.2022.966439
PMID36032250
OpenAlexW4291156127
LanguageEN
References cited7

Brain structural abnormalities have been demonstrated in schizophrenia (SZ); these resemble those seen in typical aging, but are seen at younger ages. Furthermore, SZ is associated with accelerated global brain aging, as measured by brain structure-based brain predicted age difference (Brain-PAD). High heterogeneity exists in the degree of brain abnormalities in SZ, and individual differences may be related to levels of peripheral inflammation and may relate to cognitive deficits and negative symptoms. The goal of our study was to investigate the relationship between brain aging, peripheral inflammation, and symptoms of SZ. We hypothesized older brain-PAD in SZ vs. healthy comparison (HC) participants, as well as positive relationships of brain-PAD with peripheral inflammation markers and symptoms in SZ. We analyzed data from two cross-sectional studies in SZ ( n = 26; M/F: 21/5) and HC ( n = 28; 20/8) (22-64 years). Brain-PAD was calculated using a previously validated Gaussian process regression model applied to raw T1-weighted MRI data. Plasma levels of inflammatory biomarkers (CRP, Eotaxin, Fractalkine, IP10, IL6, IL10, ICAM1, IFNγ, MCP1, MIP1β, SAA, TNFα, VEGF, VCAM1) and cognitive and negative symptoms were assessed. We observed a higher brain-PAD in SZ vs. HC, and advanced brain age relative to chronological age was related to higher peripheral levels of TNFα in the overall group and in the SZ group; other inflammatory markers were not related to brain-PAD. Within the SZ group, we observed no association between cognitive or negative symptoms and brain-PAD. These results support our hypothesis of advanced brain aging in SZ. Furthermore, our findings on the relationship of the pro-inflammatory cytokine TNFα with higher brain-PAD of SZ are relevant to explain heterogeneity of brain ages in SZ, but we did not find strong evidence for cognitive or negative symptom relationships with brain-PAD

Aging brain · Brain aging · Cognitive decline · Dementia · Disease · Inflammation · Peripheral · Psychiatry · Schizophrenia (object-oriented programming · Gut microbiota and health · Medicine · Neuroinflammation and Neurodegeneration Mechanisms · Tryptophan and brain disorders · Internal Medicine

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