ArticleAlpha psychiatry2026
Article in Alpha psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Schizophrenia is a complex mental disorder with an estimated heritability of 80%, yet its underlying pathophysiology remains poorly understood. Emerging evidence implicates the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) glutamate receptor-a key player in fast excitatory synaptic transmission, encoded by Glutamate Ionotropic Receptor AMPA Type Subunits 1-4 ( Methods: We conducted a participant-level meta-analysis of seven postmortem brain sample datasets (n = 295; 151 schizophrenia, 144 controls) and analyzed an independent organoid dataset (n = 16). Expression differences between schizophrenia and control samples were quantified using Hedges' g under a random-effects model, with heterogeneity assessed using the I Results: Our analysis revealed significant downregulation of all four Conclusions: Our findings highlight AMPA receptor dysfunction as a potential contributor to schizophrenia pathophysiology in a subgroup of patients, consistent with the broader role of glutamatergic signaling disruption in this disorder. The convergent evidence from postmortem brain tissue and developmental models underscores the need for further investigation of
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.