The developing brain: pathway disruptions contributing to Autism and Intellectual Disabilities

Neurodevelopment follows a complex sequence of cellular, molecular, and behavioral milestones that shape cognitive and social functioning. In autism spectrum disorders (ASD) and intellectual disabilities (ID), these processes are disrupted, leading to atypical brain connectivity, altered synaptic plasticity, and imbalances in excitatory and inhibitory signaling, among others. Emerging research highlights the roles of genetic mutations, epigenetic modifications, and neuroinflammatory processes in shaping the neurodevelopmental trajectory of ASD and ID.

At the cellular and molecular level, deviations in neuronal migration, synaptogenesis, and neurotransmitter system maturation contribute to the heterogeneity of these conditions. Dysregulation in pathways involving glutamatergic, GABAergic, and neuromodulatory systems has been implicated in the core features of ASD and ID, including deficits in social interaction, communication, and cognitive flexibility.

This Research Topic aims to bring together research and reviews exploring neurodevelopmental, cellular, and molecular mechanisms underlying ASD and ID. We welcome studies that explore sub-themes such as:

1) How do specific genetic mutations affect neuronal development and circuit formation in these disorders?

2) What are the cellular and molecular mechanisms underlying synaptic dysfunction in ASD and ID?

3) How does excitatory/inhibitory imbalance contribute to behavioral phenotypes in neurodevelopmental disorders?

4) What is the role of neurotransmitter systems—such as glutamate, GABA, dopamine, and serotonin—in the pathophysiology of ASD and ID?

5) How do epigenetic modifications influence brain development in individuals with ASD and ID?

6) What are the contributions of neuroinflammation and immune system dysregulation to these conditions?

7) Can early deviations in brain connectivity serve as biomarkers for ASD and ID?

8) What novel molecular targets are being explored for therapeutic intervention?

9) How can translational models help bridge preclinical findings and clinical applications in ASD and ID research?