Evidence map›Paper›PMID 41258376›Full record

SynthesisMolecular psychiatry2026

Molecular and topographic mapping of antipsychotic effects: a meta-analysis of postsynaptic density proteins in animal models with translational implications.

Giuseppe De Simone, Michele De Prisco, Vincenzo Oliva, Licia Vellucci, Mariateresa Ciccarelli, Benedetta Mazza, Giovanna Fico, Michele Fornaro, Felice Iasevoli, Eduard Vieta and 1 more

Abstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Molecular 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.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Giuseppe De Simone *Section of Psychiatry. Laboratory of Molecular and Translational Psychiatry. Unit of Treatment-Resistant Psychiatric Disorders. Department of Neuroscience, Reproductive Sciences and Dentistry, University of Naples "Federico II", School of Medicine, via Pansini 5, 80131, Naples, Italy.ORCID http://orcid.org/0000-0003-0422-3415
Michele De Prisco *Bipolar and Depressive Disorders Unit, Hospìtal Clinic de Barcelona, c. Villarroel, 170, 08036, Barcelona, Spain.ORCID http://orcid.org/0000-0002-2032-1181
Vincenzo OlivaBipolar and Depressive Disorders Unit, Hospìtal Clinic de Barcelona, c. Villarroel, 170, 08036, Barcelona, Spain.ORCID http://orcid.org/0000-0002-5961-6032
Licia VellucciSection of Psychiatry. Laboratory of Molecular and Translational Psychiatry. Unit of Treatment-Resistant Psychiatric Disorders. Department of Neuroscience, Reproductive Sciences and Dentistry, University of Naples "Federico II", School of Medicine, via Pansini 5, 80131, Naples, Italy.
Mariateresa CiccarelliSection of Psychiatry. Laboratory of Molecular and Translational Psychiatry. Unit of Treatment-Resistant Psychiatric Disorders. Department of Neuroscience, Reproductive Sciences and Dentistry, University of Naples "Federico II", School of Medicine, via Pansini 5, 80131, Naples, Italy.ORCID http://orcid.org/0000-0001-8944-414X
Benedetta MazzaSection of Psychiatry. Laboratory of Molecular and Translational Psychiatry. Unit of Treatment-Resistant Psychiatric Disorders. Department of Neuroscience, Reproductive Sciences and Dentistry, University of Naples "Federico II", School of Medicine, via Pansini 5, 80131, Naples, Italy.
Giovanna FicoBipolar and Depressive Disorders Unit, Hospìtal Clinic de Barcelona, c. Villarroel, 170, 08036, Barcelona, Spain.ORCID http://orcid.org/0000-0003-1785-7126
Michele FornaroSection of Psychiatry. Laboratory of Molecular and Translational Psychiatry. Unit of Treatment-Resistant Psychiatric Disorders. Department of Neuroscience, Reproductive Sciences and Dentistry, University of Naples "Federico II", School of Medicine, via Pansini 5, 80131, Naples, Italy.ORCID http://orcid.org/0000-0002-9647-0853
Felice IasevoliSection of Psychiatry. Laboratory of Molecular and Translational Psychiatry. Unit of Treatment-Resistant Psychiatric Disorders. Department of Neuroscience, Reproductive Sciences and Dentistry, University of Naples "Federico II", School of Medicine, via Pansini 5, 80131, Naples, Italy.ORCID http://orcid.org/0000-0002-7051-5013
Eduard VietaBipolar and Depressive Disorders Unit, Hospìtal Clinic de Barcelona, c. Villarroel, 170, 08036, Barcelona, Spain.ORCID http://orcid.org/0000-0002-0548-0053
Andrea de BartolomeisSection of Psychiatry. Laboratory of Molecular and Translational Psychiatry. Unit of Treatment-Resistant Psychiatric Disorders. Department of Neuroscience, Reproductive Sciences and Dentistry, University of Naples "Federico II", School of Medicine, via Pansini 5, 80131, Naples, Italy. adebarto@unina.it.ORCID http://orcid.org/0000-0002-3188-5652

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhile antipsychotics primarily target dopamine D

methodsWe systematically reviewed and meta-analyzed peer-reviewed preclinical studies reporting quantitative effects of typical and atypical antipsychotics on PSD-related outcomes. Statistical analyses used random-effects models, with heterogeneity assessed via τ², I², and Cochran's Q. Separate meta-analyses were conducted for PSD protein type, brain region, animal type, and treatment paradigms. Meta-regressions assessed the impact of cofounding variables.

resultsWe included 81 studies (n = 2542; rodents=2510; monkeys=26), resulting in 226 meta-analyses. Both typical and atypical antipsychotics modulated PSD molecules albeit with different degree due to the drug receptor profile, dose, specific protein detected, brain region, and administration regimen. Haloperidol, amisulpride, and aripiprazole significantly increased PSD protein expression in the striatum. Acute olanzapine increased PSD molecules levels in striatal regions, reducing Arc expression in frontal cortex (SMD [95%CIs]=-2.15 [-2.7;-1.61], p < 0.0001); chronic treatment had opposite effects. Clozapine increased Homer1a levels in dorsal (1.13 [0.41;1.86], p = 0.002) and ventral striatum (1.48 [0.72;2.24], p = 0.0001), and cingulate cortex (2.12 [1.12;3.12], p < 0.0001), as well as increased NMDAR subunits levels in frontal cortex.

Indexed as

Antipsychotic AgentsAnimalsBrainDisease Models, AnimalHumansNerve Tissue ProteinsPost-Synaptic DensitySchizophreniaTranslational Research, BiomedicalAntipsychotic AgentsNerve Tissue Proteinspostsynaptic density proteins

Identifiers

PMID41258376
PMCPMC12815681

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