Evidence map›Paper›PMID 28758643›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2018

Complement Gene Expression Correlates with Superior Frontal Cortical Thickness in Humans.

Dana M Allswede, Amanda B Zheutlin, Yoonho Chung, Kevin Anderson, Christina M Hultman, Martin Ingvar, Tyrone D Cannon

Open access · hybridAbstract readTwin Study
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 43 citations in OpenAlex.

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  3. Spatial multiomics of arterial regions from cardiac allograft vasculopathy rejected grafts reveal novel insights into the pathogenesis of chronic antibody-mediated rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024
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  14. Aberrant Complement System Activation in Neurological Disorders.International journal of molecular sciences · 2021
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Dana M AllswedeDepartment of Psychology, Yale University.
Amanda B ZheutlinDepartment of Psychology, Yale University.
Yoonho ChungDepartment of Psychology, Yale University.
Kevin AndersonDepartment of Psychology, Yale University.
Christina M HultmanDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Sweden.
Martin IngvarDepartment of Clinical Neuroscience, Karolinska Institutet, Sweden.
Tyrone D CannonDepartment of Psychology, Yale University.
Yale University · USKarolinska Institutet · SE

Funding

Neural Phenotypes for Schizophrenia and Bipolar DisorderR01MH052857 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI CANNON, TYRONE D · 1995 to 2010
$5.0M
NIMH NIH HHS R01 MH052857
6 · The paper itself

Abstract

Recent work suggests that genes encoding complement proteins that are active in the innate immune system may confer risk for schizophrenia by disrupting typical synaptic pruning in late adolescence. Alterations in the complement pathway may contribute to aberrant cortical thinning in schizophrenia prodromes and reduced prefrontal cortical thickness in chronic schizophrenia patients; however, this theory needs to be translated to humans. We conducted a series of analyses in a sample of adult Swedish twins enriched for schizophrenia (N=129) to assess the plausibility of a relationship between complement gene expression and cortical thickness that could go awry in the etiology of schizophrenia. First, we identified that peripheral mRNA expression levels of two complement genes (C5, SERPING1) made unique contributions to the variance in superior frontal cortical thickness among all participants. Vertex-wise maps of the association between gene expression levels and thickness across the cortex suggested that this relationship was especially strong with SERPING1 in the superior frontal region, consistent with the pattern of disruption in cortical thickness observed in schizophrenia. Additional analyses identified that these genes are expressed in the human superior frontal cortex, that heritable genetic factors influence SERPING1 gene expression levels, and that these associations are observed regardless of case status. These findings provide initial evidence linking the complement system with cortical thinning in humans, a process potentially involved in the pathogenesis of schizophrenia.

Indexed as

AdultAgedComplement C1 Inhibitor ProteinComplement C5FemaleFrontal LobeGene ExpressionHumansMagnetic Resonance ImagingMaleMicroarray AnalysisMiddle AgedOrgan SizeRNA, MessengerSchizophreniaComplement C1 Inhibitor ProteinComplement C5RNA, MessengerSERPING1 protein, human

Identifiers

PMID28758643
PMCPMC5770755
OpenAlexW2740432425

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.