ReviewFrontiers in psychiatry2018
A Mini Review on the Contribution of the Anterior Cingulate Cortex in the Risk of Psychosis in 22q11.2 Deletion Syndrome.
Review in Frontiers in psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Molecular and immunological origins of catatonia.Schizophrenia research · 2024Article
- Opposing white matter microstructure abnormalities in 22q11.2 deletion and duplication carriers.Translational psychiatry · 2021Article
- Pathways to understanding psychosis through rare - 22q11.2DS - and common variants.Current opinion in genetics & development · 2021Review
- Structural control energy of resting-state functional brain states reveals less cost-effective brain dynamics in psychosis vulnerability.Human brain mapping · 2021Article
- Neuroimaging Phenotypes Associated With Risk and Resilience for Psychosis and Autism Spectrum Disorders in 22q11.2 Microdeletion Syndrome.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2021Review
- Brain morphometry in 22q11.2 deletion syndrome: an exploration of differences in cortical thickness, surface area, and their contribution to cortical volume.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
22q11.2 deletion syndrome (22q11DS) is a neurogenetic disorder that causes a high risk of developing schizophrenia, thus representing a unique model for the investigation of biomarkers of psychosis. Cognitive and clinical risk factors have been identified as reliable predictors of schizophrenia in patients with 22q11DS and are currently used in the clinical practice. However, biomarkers based on neuroimaging are still lacking, mainly because of the analytic approaches adopted so far, which are almost uniquely based on the comparison of 22q11DS patients with healthy controls. Such comparisons do not take into account the heterogeneity within patients with 22q11DS, who indeed show various clinical manifestations. More recently, a number of studies compared measures of brain morphology and connectivity between patients with 22q11DS with different symptomatic profiles. The aim of this short review is to highlight the brain alterations found in patients with 22q11DS fulfilling ultra-high risk (UHR) criteria. Findings point to alterations in brain morphology and connectivity in frontal brain regions, and in particular in the anterior cingulate cortex, in patients with 22q11DS presenting UHR symptoms. These alterations may represent valuable biomarkers of psychosis in 22q11DS.
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