Evidence map›Paper›PMID 37328766›Full record

ReviewJournal of neurodevelopmental disorders2023

Event-related potential (ERP) markers of 22q11.2 deletion syndrome and associated psychosis.

Ana A Francisco, John J Foxe, Sophie Molholm

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neurodevelopmental disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Neurobiology of schizophrenia.Current opinion in neurobiology · 2024
    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

3 authors at 1 institution in 2 countries.

Ana A FranciscoDepartment of Pediatrics, The Cognitive Neurophysiology Laboratory, Albert Einstein College of Medicine, Bronx, NY, USA. claraafrancisco@gmail.com.ORCID 0000-0003-4030-0297
John J FoxeDepartment of Pediatrics, The Cognitive Neurophysiology Laboratory, Albert Einstein College of Medicine, Bronx, NY, USA.
Sophie MolholmDepartment of Pediatrics, The Cognitive Neurophysiology Laboratory, Albert Einstein College of Medicine, Bronx, NY, USA. sophie.molholm@einsteinmed.edu.
Albert Einstein College of Medicine · US

Funding

SUPPORT FOR THE ROSE F KENNEDY IDDRC P50P50HD105352 · NICHD · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Julie Secombe · 2021 to 2026
$7.0M
Support for the Rose F. Kennedy IDDRCU54HD090260 · NICHD · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI GREALLY, JOHN · 2016 to 2020
$6.0M
NICHD NIH HHS P50 HD105352NICHD NIH HHS U54 HD090260
6 · The paper itself

Abstract

22q11.2 deletion syndrome (22q11.2DS) is a multisystemic disorder characterized by a wide range of clinical features, ranging from life-threatening to less severe conditions. One-third of individuals with the deletion live with mild to moderate intellectual disability; approximately 60% meet criteria for at least one psychiatric condition.22q11.2DS has become an important model for several medical, developmental, and psychiatric disorders. We have been particularly interested in understanding the risk for psychosis in this population: Approximately 30% of the individuals with the deletion go on to develop schizophrenia. The characterization of cognitive and neural differences between those individuals who develop schizophrenia and those who do not, despite being at genetic risk, holds important promise in what pertains to the clarification of paths to disease and to the development of tools for early identification and intervention.Here, we review our previous event-related potential (ERP) findings as potential markers for 22q11.2DS and the associated risk for psychosis, while discussing others' work. We focus on auditory processing (auditory-evoked potentials, auditory adaptation, and auditory sensory memory), visual processing (visual-evoked potentials and visual adaptation), and inhibition and error monitoring.The findings discussed suggest basic mechanistic and disease process effects on neural processing in 22q11.2DS that are present in both early sensory and later cognitive processing, with possible implications for phenotype. In early sensory processes, both during auditory and visual processing, two mechanisms that impact neural responses in opposite ways seem to coexist-one related to the deletion, which increases brain responses; another linked to psychosis, decreasing neural activity. Later, higher-order cognitive processes may be equally relevant as markers for psychosis. More specifically, we argue that components related to error monitoring may hold particular promise in the study of risk for schizophrenia in the general population.

Indexed as

DiGeorge SyndromePsychotic DisordersSchizophreniaBrainEvoked PotentialsHumansDiGeorge syndromeEEGError monitoringResponse inhibitionSchizophreniaSensory processingVelo-cardio-facial syndrome

Identifiers

PMID37328766
PMCPMC10273715
OpenAlexW4380987377

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.