Evidence map›Paper›PMID 25902861›Full record

ArticleMolecular neurobiology2016

Hippocampal Pruning as a New Theory of Schizophrenia Etiopathogenesis.

Enrico Cocchi, Antonio Drago, Alessandro Serretti

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Plasma proteomic profile of inflammatory depressive symptoms.Brain, behavior, & immunity - health · 2026
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  5. Future avenues inLearning & memory (Cold Spring Harbor, N.Y.) · 2024
    Review
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  15. Shep regulatesDevelopment (Cambridge, England) · 2018
    Article
  16. Review
  17. Article
  18. Genetics of Aggression in Alzheimer's Disease (AD).Frontiers in aging neuroscience · 2017
    Article
  19. Article
  20. 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 2 institutions in 1 country.

Enrico CocchiDepartment of Biomedical and NeuroMotor Sciences, University of Bologna, Bologna, Italy.
Antonio DragoIRCCS Centro S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy.
Alessandro SerrettiDepartment of Biomedical and NeuroMotor Sciences, University of Bologna, Bologna, Italy. alessandro.serretti@unibo.it.
University of Bologna · ITCentro San Giovanni di Dio Fatebenefratelli · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pruning in neurons has been suggested to be strongly involved in Schizophrenia's (SKZ) etiopathogenesis in recent biological, imaging, and genetic studies. We investigated the impact of protein-coding genes known to be involved in pruning, collected by a systematic literature research, in shaping the risk for SKZ in a case-control sample of 9,490 subjects (Psychiatric Genomics Consortium). Moreover, their modifications through evolution (humans, chimpanzees, and rats) and subcellular localization (as indicative of their biological function) were also investigated. We also performed a biological pathways (Gene Ontology) analysis. Genetics analyses found four genes (DLG1, NOS1, THBS4, and FADS1) and 17 pathways strongly involved in pruning and SKZ in previous literature findings to be significantly associated with the sample under analysis. The analysis of the subcellular localization found that secreted genes, and so regulatory ones, are the least conserved through evolution and also the most associated with SKZ. Their cell line and regional brain expression analysis found that their areas of primary expression are neuropil and the hippocampus, respectively. At the best of our knowledge, for the first time, we were able to describe the SKZ neurodevelopmental hypothesis starting from a single biological process. We can also hypothesize how alterations in pruning fine regulation and orchestration, strongly related with the evolutionary newest (and so more sensitive) secreted proteins, may be of particular relevance in the hippocampus. This early alteration may lead to a mis-structuration of neural connectivity, resulting in the different brain alteration that characterizes SKZ patients.

Indexed as

Models, NeurologicalNeuronal PlasticityAnimalsCell LineDelta-5 Fatty Acid DesaturaseGene Expression RegulationGenetic Association StudiesGenomicsHippocampusHumansPolymorphism, Single NucleotideSchizophreniaSubcellular FractionsDelta-5 Fatty Acid DesaturaseComparative genomicsEnrichment analysisEtiopathogenesisEvolutive geneticsGene setGeneticsMolecular pathwaysPruningSchizophrenia

Identifiers

PMID25902861
OpenAlexW2076387780

What OpenQuestion 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 OpenQuestion graph.