Journal
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
Volume 267, Issue 5, Pages 479-483Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00406-017-0802-1
Keywords
BDNF-TrkB signaling; Cognitive deficits; Psychosis; Prevention
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Funding
- (JSPS) (Tokyo, Japan) [16F14711]
- Postdoctoral Fellowship for Overseas Researchers of JSPS (Tokyo, Japan)
- Grants-in-Aid for Scientific Research [16F14711] Funding Source: KAKEN
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Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin receptor kinase B (TrkB) signaling plays a key role in the brain neurodevelopment. The exposure of pregnant mice to polyinosinic-polycytidylic acid [poly(I:C)] causes cognitive deficits in adult offspring. Supplementation with a TrkB agonist, 7,8-dihydroxyflavone, in poly(I:C)-treated pregnant mice from pregnancy to weaning could prevent the onset of cognitive deficits and reduced BDNF-TrkB signaling in the prefrontal cortex of their adult offspring. These findings suggest that supplementation with a TrkB agonist in pregnant women with an ultra-high risk of psychosis may reduce the development of psychosis in their offspring.
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