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Prenatal Exposure to Azadiradione Leads to Developmental Disabilities
Sudipta Jana1, Sagarika Das1, Bhaskarjyoti Giri1
1Neurobiology of Disease Laboratory, Department of Bioscience and Biotechnology, Indian Institute of Technology, Kharagpur, 721302, India.
Molecular Neurobiology
|September 23, 2024
Summary
Prenatal exposure to azadiradione, a compound from neem, caused developmental disabilities in mice by increasing Ube3a expression. These deficits, including cognitive impairments, persisted into adulthood.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Azadiradione is a brain-permeable phytochemical from Azadirachta Indica (neem).
- Azadiradione induces Ube3a (ubiquitin ligase) expression, implicated in neurodevelopmental disorders.
Purpose of the Study:
- To investigate the effects of in utero azadiradione exposure on mouse development.
- To explore the role of Ube3a in azadiradione-induced developmental deficits.
Main Methods:
- Pregnant dams were treated with azadiradione at embryonic days 12 and 14.
- Newborn pups were assessed for body weight, cognitive, motor, and anxiety-like behaviors.
- Brain tissue was analyzed for Ube3a levels, target proteins, and dendritic spine density.
Main Results:
- Prenatal azadiradione exposure led to decreased pup body weight and significant cognitive, motor, and communication deficits.
- Adult mice showed persistent cognitive deficits despite partial recovery of other behaviors.
- Increased Ube3a levels and target proteins, along with enhanced dendritic spines, were observed in the brains of exposed mice.
Conclusions:
- In utero azadiradione exposure causes lasting developmental disabilities in mice.
- Elevated Ube3a expression is a key factor in azadiradione-induced neurodevelopmental issues.
- Azadiradione's impact on Ube3a highlights potential risks during pregnancy.
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