Prenatal THC Activated Schizophrenia-Linked Genes in Rat Placentas
Rats exposed to THC during pregnancy had growth-restricted offspring and placentas showing altered expression of genes previously linked to schizophrenia in human studies — with some changes differing between male and female offspring.
Quick Facts
What This Study Found
This study tested whether prenatal THC exposure in rats would alter the same placental genes that human genomic studies have linked to schizophrenia risk. The researchers administered oral THC during pregnancy and examined both fetal outcomes and placental gene expression.
THC-exposed offspring had significantly reduced fetal weights — in both males and females — without affecting maternal pregnancy outcomes. This fetal growth restriction pattern matches earlier findings in this model that THC-exposed rat offspring later develop schizophrenia-like behaviors (such as decreased pre-pulse inhibition of the acoustic startle response).
Critically, placentas from THC-exposed pregnancies showed altered expression of specific genes — Furin, Rccd1, and Atp5mk — that had been previously identified in human transcriptomic datasets as markers associated with schizophrenia. Some gene expression changes were sex-specific, affecting different genes in male versus female placentas (including Eif5, Rps10, and Vps33b).
This represents the first demonstration that prenatal THC exposure activates the same placental molecular signature that human studies have associated with schizophrenia risk.
Key Numbers
Significantly reduced fetal weights in both male and female THC-exposed offspring. No significant changes in maternal outcomes. Altered expression of Furin, Rccd1, and Atp5mk in both sexes. Sex-specific changes in Eif5, Rps10, Vps33b, and others. All target genes previously identified in human schizophrenia transcriptomic datasets.
How They Did This
Preclinical study administering oral THC to pregnant rats. Outcomes included fetal weights, maternal pregnancy outcomes, and placental gene expression analysis. Target genes were selected based on prior human transcriptomic datasets identifying placental markers of schizophrenia. Gene expression compared between THC-exposed and control placentas, analyzed separately by offspring sex.
Why This Research Matters
This study bridges two previously separate bodies of research: the human genetic studies linking placental gene signatures to schizophrenia risk, and the animal studies showing prenatal THC causes schizophrenia-like behaviors in offspring. Finding the same genes altered in both contexts strengthens the biological plausibility of a pathway from prenatal cannabis exposure through placental disruption to later psychotic illness.
The Bigger Picture
This is a mechanistic puzzle piece connecting prenatal THC exposure to the psychosis literature (RTHC-00251 on cannabis-induced psychosis converting to schizophrenia, RTHC-00163, RTHC-00201, RTHC-00203). It also adds a placental dimension to the prenatal cannabis research (RTHC-00236 on brain MRI trajectories, RTHC-00226 on molecular brain changes, RTHC-00241 on brain connectivity). The implication is that THC may not need to directly reach the fetal brain to affect neurodevelopment — it may alter placental function in ways that independently increase schizophrenia risk.
What This Study Doesn't Tell Us
Animal model — rat placental biology differs from human. Oral THC dosing may not match human exposure patterns. The correlation between altered gene expression and actual disease development is not established in this study. The specific genes identified as schizophrenia-linked in human datasets may have different functions in rat placentas. Small sample size typical of gene expression studies.
Questions This Raises
- ?Do these placental gene changes predict which offspring actually develop schizophrenia-like behaviors?
- ?Could placental biomarkers from these genes serve as early warning signs in human pregnancies?
- ?Does the timing of THC exposure during pregnancy determine which genes are affected?
Trust & Context
- Key Stat:
- Evidence Grade:
- Preclinical animal study with targeted gene expression analysis — provides important mechanistic evidence but requires human placental studies to confirm translational relevance.
- Study Age:
- Published in 2026, representing a new line of inquiry connecting prenatal THC exposure to schizophrenia through placental gene expression.
- Original Title:
- Identifying established human placental markers of schizophrenia in rodents after gestational ∆9-tetrahydrocannabinol exposure†.
- Published In:
- Biology of reproduction, 114(1), 246-258 (2026) — Biology of Reproduction is a peer-reviewed journal focusing on reproductive biology and related fields.
- Authors:
- Kocsis, Andrea M, Perez-Valenzuela, Enzo, Rodríguez-Ruiz, Mar(5), Sarikahya, Mohammed H, Dembla, Anubha, Natale, David R C, Laviolette, Steven R, Hardy, Daniel B
- Database ID:
- RTHC-08393
Evidence Hierarchy
Watches what happens naturally without intervening.
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Cite This Study
https://rethinkthc.com/research/RTHC-08393APA
Kocsis, Andrea M; Perez-Valenzuela, Enzo; Rodríguez-Ruiz, Mar; Sarikahya, Mohammed H; Dembla, Anubha; Natale, David R C; Laviolette, Steven R; Hardy, Daniel B. (2026). Identifying established human placental markers of schizophrenia in rodents after gestational ∆9-tetrahydrocannabinol exposure†.. Biology of reproduction, 114(1), 246-258. https://doi.org/10.1093/biolre/ioaf191
MLA
Kocsis, Andrea M, et al. "Identifying established human placental markers of schizophrenia in rodents after gestational ∆9-tetrahydrocannabinol exposure†.." Biology of reproduction, 2026. https://doi.org/10.1093/biolre/ioaf191
RethinkTHC
RethinkTHC Research Database. "Identifying established human placental markers of schizophr..." RTHC-08393. Retrieved from https://rethinkthc.com/research/kocsis-2026-identifying-established-human-placental
Access the Original Study
Study data sourced from PubMed, a service of the U.S. National Library of Medicine, National Institutes of Health.
This study breakdown was produced by the RethinkTHC research team. We analyze and report published research findings without making health recommendations. All interpretations are based solely on the published abstract and study data.