Evidence map›Paper›PMID 32152472›Full record

ArticleMolecular psychiatry2021

Hippocampal subfield transcriptome analysis in schizophrenia psychosis.

Jessica Marie Perez, Stefano Berto, Kelly Gleason, Subroto Ghose, Chunfeng Tan, Tae-Kyung Kim, Genevieve Konopka, Carol A Tamminga

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 4 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

23 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Trial
  6. Alpha psychiatry · 2026
    Article
  7. Article
  8. Schizophrenia.Nature reviews. Disease primers · 2025
    Review
  9. Article
  10. Pharmacological reduction of reverse-translated hippocampal hyperactivity in mouse: relevance for psychosis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
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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

8 authors.

Jessica Marie PerezDivision of Translational Neuroscience in Schizophrenia, Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA. Jessicapere18@gmail.com.
Stefano BertoDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX, 75390, USA.
Kelly GleasonDivision of Translational Neuroscience in Schizophrenia, Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Subroto GhoseDivision of Translational Neuroscience in Schizophrenia, Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Chunfeng TanDivision of Translational Neuroscience in Schizophrenia, Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Tae-Kyung KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk, 37673, Korea.ORCID http://orcid.org/0000-0001-5161-9864
Genevieve KonopkaDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX, 75390, USA.ORCID http://orcid.org/0000-0002-3363-7302
Carol A TammingaDivision of Translational Neuroscience in Schizophrenia, Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.

Funding

Basic Science Training Program in the Neurobiology of Mental IllnessT32MH076690 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI TAMMINGA, CAROL A · 2007 to 2017
$2.3M
NIMH NIH HHS T32 MH076690
6 · The paper itself

Abstract

We have previously demonstrated functional and molecular changes in hippocampal subfields in individuals with schizophrenia (SZ) psychosis associated with hippocampal excitability. In this study, we use RNA-seq and assess global transcriptome changes in the hippocampal subfields, DG, CA3, and CA1 from individuals with SZ psychosis and controls to elucidate subfield-relevant molecular changes. We also examine changes in gene expression due to antipsychotic medication in the hippocampal subfields from our SZ ON- and OFF-antipsychotic medication cohort. We identify unique subfield-specific molecular profiles in schizophrenia postmortem samples compared with controls, implicating astrocytes in DG, immune mechanisms in CA3, and synaptic scaling in CA1. We show a unique pattern of subfield-specific effects by antipsychotic medication on gene expression levels with scant overlap of genes differentially expressed by SZ disease effect versus medication effect. These hippocampal subfield changes serve to confirm and extend our previous model of SZ and can explain the lack of full efficacy of conventional antipsychotic medication on SZ symptomatology. With future characterization using single-cell studies, the identified distinct molecular profiles of the DG, CA3, and CA1 in SZ psychosis may serve to identify further potential hippocampal-based therapeutic targets.

Indexed as

Psychotic DisordersSchizophreniaGene Expression ProfilingHippocampusHumansMagnetic Resonance Imaging

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.