Abstract

Neuronal surface autoantibody-mediated encephalitis (NSAME) is a complex and rapidly emerging field of neuroimmunology characterized by immune-mediated attacks on neuronal cell surface antigens. This abstract provides an overview of the pathogenic pathways underlying NSAME, summarizing key mechanisms and factors contributing to disease development. NSAME is associated with a wide spectrum of clinical manifestations, often presenting with a range of neurological and psychiatric symptoms. Central to the pathogenesis of NSAME are autoantibodies targeting specific neuronal surface proteins, such as NMDA receptors, LGI1, CASPR2, and GABA (B) receptors, among others. These autoantibodies disrupt synaptic transmission, induce receptor internalization, and trigger inflammatory responses in the central nervous system. Additionally, genetic predisposition, environmental triggers, and dysregulated immune responses play pivotal roles in disease initiation and progression. This abstract aims to elucidate the intricate interplay between autoimmunity, neuroinflammation, and neuronal dysfunction in NSAME, shedding light on potential therapeutic strategies for this challenging neurological disorder. Understanding these pathogenic pathways is critical for advancing the diagnosis, treatment, and management of NSAME and improving the quality of life for affected individuals.