Evidence map›Paper›PMID 36844807›Full record

ArticleRoyal Society open science2023

Genomic insights into schizophrenia.

Michael J Owen

Abstract read
In one paragraph

Article in Royal Society open science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
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

1 author.

Michael J OwenCentre for Neuropsychiatric Genetics and Genomics, Neuroscience and Mental Health Innovation Institute and Division of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff CF10 3AT, UK.ORCID 0000-0003-4798-0862

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is a common, complex, heterogeneous psychiatric syndrome which can have profound impacts on affected individuals and imposes significant burdens on society. Despite intensive research, it has been challenging to understand basic mechanisms and to identify novel therapeutic targets. Given its high heritability and the complexity and inaccessibility of the human brain, much hope has been invested in the application of genomics as a route to better understanding. This work has identified many common and rare risk alleles and laid the foundations for a new generation of mechanistic studies. Genomics has also thrown new light on the relationship between schizophrenia and other psychiatric disorders and revealed its previously unappreciated aetiological relationship with childhood neurodevelopmental disorders, providing further evidence that it has its origins in disturbances of brain development. In addition, genomic findings suggest that the condition reflects fundamental disturbances in neuronal, and particularly synaptic, function that impact broadly on brain function, rather than being a disorder of specific brain regions and circuits. Finally, genomics has provided a plausible solution to the evolutionary paradox of how the condition persists in the face of high heritability and reduced fecundity.

Indexed as

evolutiongenomicsneurobiologyneurodevelopmentschizophrenia

Identifiers

PMID36844807
PMCPMC9943879

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.