Evidence map›Paper›PMID 25311587›Full record

ReviewNature reviews. Neurology2014

Maternal immune activation and abnormal brain development across CNS disorders.

Irene Knuesel, Laurie Chicha, Markus Britschgi, Scott A Schobel, Michael Bodmer, Jessica A Hellings, Stephen Toovey, Eric P Prinssen

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03848481 (Cannabidivarin), which is not on this map. Cited by 492 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
492citing papers in PubMed, 3 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.

NCT03848481 phase2terminatednot on this mapstarted 2020, after this paper: background citation

Cannabidivarin (CBDV) vs. Placebo in Children and Adults up to Age 30 With Prader-Willi Syndrome (PWS)

TypeinterventionalSponsorEric HollanderRan2020 to 2024Enrolled6ConditionsPrader-Willi SyndromeArmsCBDV Compound, Placebo
3 · Its place in the literature

Who cites it

492 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. The Effects of Malaria in Pregnancy on Neurocognitive Development in Children at 1 and 6 Years of Age in Benin: A Prospective Mother-Child Cohort.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022
    Trial
  6. Review
  7. Article
  8. Article
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  13. Review
  14. Article
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  16. Article
  17. Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026
    Review
  18. Article
  19. Article
  20. Article

432 more citing papers are in PubMed but not listed here.

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.

Irene KnueselRoche Pharma Research and Early Development, Roche Innovation Centre Basel, Grenzacherstrasse 124, 4070 Basel, Switzerland.
Laurie ChichaBrain Ischemia &Regeneration Group, Department of Biomedicine, University Hospital, Hebelstrasse 20, 4031 Basel, Switzerland.
Markus BritschgiRoche Pharma Research and Early Development, Roche Innovation Centre Basel, Grenzacherstrasse 124, 4070 Basel, Switzerland.
Scott A SchobelRoche Pharma Research and Early Development, Roche Innovation Centre Basel, Grenzacherstrasse 124, 4070 Basel, Switzerland.
Michael BodmerDepartment of Internal Medicine, Emergency Unit, University Hospital, Petersgraben 2, 4031 Basel, Switzerland.
Jessica A HellingsThe Nisonger Centre, Ohio State University, 1581 Dodd Drive, Columbus, OH 43210, USA.
Stephen TooveyPegasus Research, Burggartenstrasse 32, 4103 Bottmingen, Switzerland.
Eric P PrinssenRoche Pharma Research and Early Development, Roche Innovation Centre Basel, Grenzacherstrasse 124, 4070 Basel, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiological studies have shown a clear association between maternal infection and schizophrenia or autism in the progeny. Animal models have revealed maternal immune activation (mIA) to be a profound risk factor for neurochemical and behavioural abnormalities in the offspring. Microglial priming has been proposed as a major consequence of mIA, and represents a critical link in a causal chain that leads to the wide spectrum of neuronal dysfunctions and behavioural phenotypes observed in the juvenile, adult or aged offspring. Such diversity of phenotypic outcomes in the mIA model are mirrored by recent clinical evidence suggesting that infectious exposure during pregnancy is also associated with epilepsy and, to a lesser extent, cerebral palsy in children. Preclinical research also suggests that mIA might precipitate the development of Alzheimer and Parkinson diseases. Here, we summarize and critically review the emerging evidence that mIA is a shared environmental risk factor across CNS disorders that varies as a function of interactions between genetic and additional environmental factors. We also review ongoing clinical trials targeting immune pathways affected by mIA that may play a part in disease manifestation. In addition, future directions and outstanding questions are discussed, including potential symptomatic, disease-modifying and preventive treatment strategies.

Indexed as

Alzheimer DiseaseAnimalsBrainCentral Nervous System DiseasesCerebral PalsyChild Development Disorders, PervasiveFemaleHumansParkinson DiseasePregnancyPregnancy Complications, InfectiousPrenatal Exposure Delayed EffectsSchizophrenia

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.