Evidence map›Paper›PMID 28990258›Full record

ArticleHuman brain mapping2018

Baseline connectome modular abnormalities in the childhood phase of a longitudinal study on individuals with chromosome 22q11.2 deletion syndrome.

Liang Zhan, Lisanne M Jenkins, Aifeng Zhang, Giorgio Conte, Angus Forbes, Danielle Harvey, Kathleen Angkustsiri, Naomi J Goodrich-Hunsaker, Courtney Durdle, Aaron Lee and 5 more

Open access · greenAbstract read
In one paragraph

Article in Human brain mapping, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
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

15 authors at 5 institutions in 1 country.

Liang ZhanComputer Engineering Program, University of Wisconsin-Stout, Wisconsin.ORCID 0000-0002-7920-4828
Lisanne M JenkinsDepartment of Psychiatry, University of Illinois, Chicago, Illinois.ORCID 0000-0002-1241-1662
Aifeng ZhangDepartment of Psychiatry, University of Illinois, Chicago, Illinois.ORCID 0000-0003-4124-2199
Giorgio ConteDepartment of Computer Science, University of Illinois, Chicago, Illinois.
Angus ForbesDepartment of Computer Science, University of Illinois, Chicago, Illinois.
Danielle HarveyDivision of Biostatistics, Department of Public Health Sciences, School of Medicine, University of California, Davis, California.
Kathleen AngkustsiriDepartment of Pediatrics, University of California, Davis, California.
Naomi J Goodrich-HunsakerDepartment of Psychiatry and Behavioral Sciences, University of California, Davis, California.ORCID 0000-0002-0462-2910
Courtney DurdleDepartment of Psychiatry and Behavioral Sciences, University of California, Davis, California.
Aaron LeeDepartment of Psychiatry and Behavioral Sciences, University of California, Davis, California.
Cyndi SchumannDepartment of Psychiatry and Behavioral Sciences, University of California, Davis, California.
Owen CarmichaelPennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana.ORCID 0000-0002-0576-0047
Kristopher KalishDepartment of Neurology, University of California, Davis, California.
Alex D LeowDepartment of Psychiatry, University of Illinois, Chicago, Illinois.
Tony J SimonDepartment of Psychiatry and Behavioral Sciences, University of California, Davis, California.
University of California, Davis · USUniversity of Illinois Chicago · USBrigham Young University · USPennington Biomedical Research Center · USUniversity of Wisconsin–Stout · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Leigh Lamonica · 2012 to 2026
$69.1M
Rodent Behavior CoreU54HD079125 · NICHD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ABBEDUTO, LEONARD J. · 2013 to 2019
$8.5M
Visuospatial Cognitive Deficit in Del22q11.2 SyndromeR01HD042974 · NICHD · UNIVERSITY OF CALIFORNIA DAVIS · PI SIMON, TONY J · 2003 to 2013
$4.9M
Cognitive-Affective Psychosis Proneness Risk and protective factors in 22q11.2DSR01MH107108 · NIMH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ANGKUSTSIRI, KATHLEEN · 2015 to 2020
$3.4M
Highly-sensitive imaging markers for early detection of Alzheimer's Disease using multi-view connectomicsR21AG056782 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LEOW, ALEX, THOMPSON, PAUL M · 2017 to 2018
$425k
NIA NIH HHS R21 AG056782NICHD NIH HHS R01 HD042974NICHD NIH HHS U54 HD079125NIGMS NIH HHS U54 GM104940NIMH NIH HHS R01 MH107108
6 · The paper itself

Abstract

Occurring in at least 1 in 3,000 live births, chromosome 22q11.2 deletion syndrome (22q11DS) produces a complex phenotype that includes a constellation of medical complications such as congenital cardiac defects, immune deficiency, velopharyngeal dysfunction, and characteristic facial dysmorphic features. There is also an increased incidence of psychiatric diagnosis, especially intellectual disability and ADHD in childhood, lifelong anxiety, and a strikingly high rate of schizophrenia spectrum disorders, which occur in around 30% of adults with 22q11DS. Using innovative computational connectomics, we studied how 22q11DS affects high-level network signatures of hierarchical modularity and its intrinsic geometry in 55 children with confirmed 22q11DS and 27 Typically Developing (TD) children. Results identified 3 subgroups within our 22q11DS sample using a K-means clustering approach based on several midline structural measures-of-interests. Each subgroup exhibited distinct patterns of connectome abnormalities. Subtype 1, containing individuals with generally healthy-looking brains, exhibited no significant differences in either modularity or intrinsic geometry when compared with TD. By contrast, the more anomalous 22q11DS Subtypes 2 and 3 brains revealed significant modular differences in the right hemisphere, while Subtype 3 (the most anomalous anatomy) further exhibited significantly abnormal connectome intrinsic geometry in the form of left-right temporal disintegration. Taken together, our findings supported an overall picture of (a) anterior-posteriorly differential interlobar frontotemporal/frontoparietal dysconnectivity in Subtypes 2 and 3 and (b) differential intralobar dysconnectivity in Subtype 3. Our ongoing studies are focusing on whether these subtypes and their connnectome signatures might be valid biomarkers for predicting the degree of psychosis-proneness risk found in 22q11DS. Hum Brain Mapp 39:232-248, 2018. © 2017 Wiley Periodicals, Inc.

Indexed as

ConnectomeAdolescentBrainChildCluster AnalysisDiGeorge SyndromeFemaleFunctional LateralityHumansLongitudinal StudiesMaleNeural Pathways22q11DSbrain connectomediffusion MRIintrinsic geometrymodularity

Identifiers

PMID28990258
PMCPMC5757536
OpenAlexW2762587098

What OpenQuestion holds

Textmetadata
LicenceTDM
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.