ReviewCurrent opinion in neurobiology2024
Polygenicity in a box: Copy number variants, neural circuit development, and neurodevelopmental disorders.
Review in Current opinion in neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.Disease models & mechanisms · 2026Article
- Driver or passenger? A new assessment of genes in the schizophrenia-associated 3q29 deletion locus for contribution to neurodevelopmental disorders.Journal of neurodevelopmental disorders · 2026Review
- Convergent effects of neurodevelopmental disorder-associated variants at mitochondria.bioRxiv : the preprint server for biology · 2026Article
- Suppressive Genetic Interactions Between Haploinsufficient Mitochondrial Genes Encoded in the 22q11.2 Microdeletion Locus Define Brain and Cardiac Phenotypes.bioRxiv : the preprint server for biology · 2026Article
- Distinct cellular and transcriptional mechanisms mediate an antioxidant therapeutic response in 22q11-deleted upper layer cortical projection neurons.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Clinically defined neurodevelopmental disorders (cd-NDDs), including Autistic Spectrum Disorder (ASD) and Schizophrenia (Scz), are primarily polygenic: Multiple risk genes distributed across the genome, in potentially infinite combinations, account for variable pathology. Polygenicity raises a fundamental question: Can "core" cd-NDD pathogenic mechanisms be identified given this genomic complexity? With the right models and analytic targets, a distinct class of polygenic mutations-Copy Number Variants (CNVs): contiguous gene deletions or duplications associated with cd-NDD risk-provide a singular opportunity to define cd-NDD pathology. CNVs orthologous to those that confer cd-NDD risk have been engineered in animals as well as human stem cells. Using these tools, one can determine how altered function of multiple genes cause serial stumbles over cell biological steps typically taken to build optimal "polygenic" neural circuits. Thus, cd-NDD pathology may be a consequence of polygenic deviations-stumbles-that exceed limits of adaptive variation for key developmental steps.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.