Evidence map›Paper›PMID 29177493›Full record

ArticleBrain : a journal of neurology2017

Calretinin interneuron density in the caudate nucleus is lower in autism spectrum disorder.

Istvan Adorjan, Bashir Ahmed, Virginia Feher, Mario Torso, Kristine Krug, Margaret Esiri, Steven A Chance, Francis G Szele

Erratum issuedOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain : a journal of neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

  1. Lower Striatal and Cortical Calretinin Interneuron Density Associated With Altered Social Behavior in Cntnap2 Knockout Mice.Autism research : official journal of the International Society for Autism Research · 2026
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  17. In vivo imaging translocator protein (TSPO) in autism spectrum disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Istvan AdorjanDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Bashir AhmedDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Virginia FeherDepartment of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Mario TorsoNuffield Department of Clinical Neuroscience, University of Oxford, Oxford, UK.
Kristine KrugDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Margaret EsiriNuffield Department of Clinical Neuroscience, University of Oxford, Oxford, UK.
Steven A ChanceNuffield Department of Clinical Neuroscience, University of Oxford, Oxford, UK.
Francis G SzeleDepartment of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
University of Oxford · GBSemmelweis University · HU

Funding

Biotechnology and Biological Sciences Research Council BB/H016902/1Medical Research Council MR/L022656/1
6 · The paper itself

Abstract

Autism spectrum disorder is a debilitating condition with possible neurodevelopmental origins but unknown neuroanatomical correlates. Whereas investigators have paid much attention to the cerebral cortex, few studies have detailed the basal ganglia in autism. The caudate nucleus may be involved in the repetitive movements and limbic changes of autism. We used immunohistochemistry for calretinin and neuropeptide Y in 24 age- and gender-matched patients with autism spectrum disorder and control subjects ranging in age from 13 to 69 years. Patients with autism had a 35% lower density of calretinin+ interneurons in the caudate that was driven by loss of small calretinin+ neurons. This was not caused by altered size of the caudate, as its cross-sectional surface areas were similar between diagnostic groups. Controls exhibited an age-dependent increase in the density of medium and large calretinin+ neurons, whereas subjects with autism did not. Diagnostic groups did not differ regarding ionized calcium-binding adapter molecule 1+ immunoreactivity for microglia, suggesting chronic inflammation did not cause the decreased calretinin+ density. There was no statistically significant difference in the density of neuropeptide Y+ neurons between subjects with autism and controls. The decreased calretinin+ density may disrupt the excitation/inhibition balance in the caudate leading to dysfunctional corticostriatal circuits. The description of such changes in autism spectrum disorder may clarify pathomechanisms and thereby help identify targets for drug intervention and novel therapeutic strategies.

Indexed as

AdolescentAdultAgedAutism Spectrum DisorderCalbindin 2Calcium-Binding ProteinsCase-Control StudiesCaudate NucleusCerebral CortexDNA-Binding ProteinsFemaleHumansInterneuronsMaleMicrofilament ProteinsMicrogliaAIF1 protein, humanCalbindin 2Calcium-Binding ProteinsDNA-Binding ProteinsMicrofilament ProteinsNeuropeptide Yautism spectrum disordermicroglianeuroinflammationneuropsychiatry

Identifiers

PMID29177493
PMCPMC6624365
OpenAlexW2733839429

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.