Neurodevelopmental disorders

Cell adhesion presence during adolescence controls the architecture of projection-defined prefrontal cortical neurons and reward-related action strategies later in life

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During teenage years, the brain undergoes important structural changes that set the stage for adult decision-making abilities. This study found that a cell adhesion protein called β1-integrin plays a critical role during adolescence in stabilizing connections between brain cells in the prefrontal cortex. When this protein was missing during the teenage years, adult mice struggled to make good decisions about rewards and could not adjust their behavior when circumstances changed. The research suggests that proper brain development during adolescence requires these cellular adhesion molecules to build the neural circuits needed for intelligent decision-making later in life.

Deciphering the role of CAPZA2 in neurodevelopmental disorders: insights from mouse models

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Scientists studied a gene called CAPZA2 that helps control how brain cells connect to each other. When this gene doesn’t work properly, mice had trouble learning, remembering things, and interacting socially, similar to intellectual disability in humans. The researchers found that the problem happens because the connections between brain cells become abnormal and don’t mature properly. This research helps explain why some people with mutations in this gene have developmental difficulties and could lead to new treatments.

Reelin cells and sex-dependent synaptopathology in autism following postnatal immune activation

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Researchers found that infections in newborn mice, particularly males, can disrupt brain development and lead to autism-like behaviors by damaging special brain cells called Reelin+ cells that help synapses mature properly. These damaged synapses failed to develop normally, resulting in social withdrawal and repetitive behaviors similar to autism in humans. Importantly, the study found that male mice were much more susceptible to this immune-triggered damage than female mice. The findings suggest that Reelin could be a promising therapeutic target for treating autism in children who experienced infections early in life.

N-terminal oligomerization drives HDAC4 nuclear condensation and neurodevelopmental dysfunction in Drosophila

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This study reveals how a protein called HDAC4 forms clumps inside cell nuclei, which damages brain development. Researchers found that the protein’s ability to stick to itself (oligomerize) drives this clumping process. By modifying the protein to prevent self-sticking, they reduced the damage to developing brain structures, suggesting new ways to treat brain disorders linked to HDAC4 accumulation.

Disease: Neurodevelopmental disorders

Cell adhesion presence during adolescence controls the architecture of projection-defined prefrontal cortical neurons and reward-related action strategies later in life

Deciphering the role of CAPZA2 in neurodevelopmental disorders: insights from mouse models

Reelin cells and sex-dependent synaptopathology in autism following postnatal immune activation

N-terminal oligomerization drives HDAC4 nuclear condensation and neurodevelopmental dysfunction in Drosophila