Characterization of Lipizzan Horse Population From Lipica Stud Using Molecular and Pedigree Data.

The establishment of precise neural circuits in the developing central nervous system (CNS) depends on highly coordinated and dynamic morphological change and/or remodeling of neuronal cells [,,,]. Throughout development, neuronal cells extend and elongate neurites, navigate toward appropriate targets, and progressively assemble synaptic connections to form organized neuronal networks [,]. Despite extensive investigation, the molecular programs that precisely regulate the sequential stages of neuronal cell morphological differentiation remain incompletely defined. Perturbations in these morphogenetic events can arise not only during early neurodevelopment but also at later stages, resulting in aberrant neuronal process extension, guidance, synapse formation, and their maintenance [,,,]. Such structural abnormalities are thought to compromise circuit assembly by disrupting intercellular connectivity and the neurite elongation required for proper integration within brain regions. In particular, dysregulated control of neuronal process elongation, which may manifest as either excessive [] or insufficient [] neurite or axonal growth based on anatomical observations, is thought to play a role in several neurological and neurodevelopmental disorders [,,,]. Evidence indicates that dysregulation of neuronal cell morphogenesis constitutes a fundamental pathogenic mechanism underlying neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD) and intellectual disability (ID), ultimately contributing to deficits in neuronal process and network formation, as well as synaptic organization [,].