Th2brain: Effects of Th2-related immunity in the postnatal maturation of brain circuits

Overview

Project Summary

Allergies, including atopic dermatitis, allergic asthma and rhinitis, are among the most prevalent chronic inflammatory disorders worldwide and share a strong comorbidity with Attention-Deficit/Hyperactivity Disorder (ADHD). We recently described a microglia-dependent mechanistic study that might justify this comorbidity. In mice, we showed that a premature increase in IL-4 (a central regulator in Th2 immunity and allergies) in early life induces an increase survival of cerebellar neurons, alters cerebellar connectivity and induces ADHD-related behaviors. The Th2brain project aims to understand how the cerebellum is susceptible to IL-4 effects and how IL-4 impacts microglia-dependent cerebellar remodeling in this critical window of postnatal cerebellar development.

Main Goals

The Th2brain aims at understanding how Th2 hyperresponsiveness leads to abnormal behaviors, why is the cerebellum susceptible to these insults and whether microglia the main cellular drivers of ADHD-like behaviors dependent on IL-4.

External Team

This project is being performed in collaboration of Judy Allen and Andrew Greenhalgh from the Lydia Becker Institute of Immunology and Inflammation from the University of Manchester.

Partners

Funding

Project Details

Project Code

2022.02604.PTDC

Start Date

2023-03-25

End Date

2026-03-24

Total Cost

€ 249 267,75

Funding Details

FCT

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