The potential and therapeutic advances of the integrin family in neurological disorders.

Neurological disorders encompass a diverse and heterogeneous group of medical conditions, including cerebrovascular diseases (e.g., stroke), neurodegenerative diseases (e.g., Alzheimer's disease and Parkinson's disease), and autoimmune demyelinating disorders (e.g., multiple sclerosis). With the global aging population, the incidence of these disorders continues to rise, posing significant challenges to healthcare systems and socio-economic structures. Recent studies have highlighted integrins-a family of transmembrane glycoprotein receptors-as critical regulators of central nervous system function, making them a focal point in neurological disease research. By interacting with the extracellular matrix, integrins modulate cell adhesion, signal transduction, and inflammatory responses, playing indispensable roles in neuronal development, synaptic plasticity, and blood-brain barrier maintenance. Dysregulated integrin signaling has been implicated in the pathophysiology of various neurological disorders, suggesting that integrin-targeting interventions, including integrin antagonists or agonists, could represent novel therapeutic strategies. Preclinical and clinical studies have demonstrated that modulating integrin function influences disease progression, offering promising avenues for the development of precision medicine approaches. This review provides a comprehensive analysis of integrin structure, classification, and their physiological and pathological roles in the central nervous system, with a focus on their molecular mechanisms in neurological disorders. Furthermore, we evaluate the therapeutic potential and challenges associated with integrin-targeted interventions. By elucidating the mechanistic underpinnings of integrin function in the central nervous system, this review aims to advance our understanding of their translational potential, laying the groundwork for the development of innovative therapeutic strategies.