Phosphodiesterase 2A inhibition corrects the aberrant behavioral traits observed in genetic and environmental preclinical models of Autism Spectrum Disorder
Schiavi S., Carbone E., Melancia F., di Masi A., Jarjat M., Brau F.
Animal Study, published in Transl Psychiatry (2022) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Transl Psychiatry (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 35338117
- PMCID
- PMC8956682
- DOI
- 10.1038/s41398-022-01885-2
- Citations
- 12
Abstract (original English)
Pharmacological inhibition of phosphodiesterase 2A (PDE2A), which catalyzes the hydrolysis of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), has recently been proposed as a novel therapeutic tool for Fragile X Syndrome (FXS), the leading monogenic cause of Autism Spectrum Disorder (ASD). Here, we investigated the role of PDE2A in ASD pathogenesis using two rat models that reflect one of either the genetic or environmental factors involved in the human disease: the genetic Fmr1- Δ exon 8 rat model and the environmental rat model based on prenatal exposure to valproic acid (VPA, 500 mg/kg). Prior to behavioral testing, the offspring was treated with the PDE2A inhibitor BAY607550 (0.05 mg/kg at infancy, 0.1 mg/kg at adolescence and adulthood). Socio-communicative symptoms were assessed in both models through the ultrasonic vocalization test at infancy and three-chamber test at adolescence and adulthood, while cognitive impairments were assessed by the novel object recognition test in Fmr1- Δ exon 8 rats (adolescence and adulthood) and by the inhibitory avoidance test in VPA-exposed rats (adulthood). PDE2A enzymatic activity in VPA-exposed infant rats was also assessed. In line with the increased PDE2A enzymatic activity previously observed in the brain of Fmr1-KO animals, we found an altered upstream regulation of PDE2A activity in the brain of VP
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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