Abnormal protein glycosylation in epileptogenesis: evidence from experimental models and clinical insights

Epilepsy is a brain disease caused by transient changes in the patients' clinical status due to excessive neuronal discharge or depolarization. Despite the increasing understanding of potential risk factors for epileptic seizures, there is still no method to prevent the onset of epilepsy in high-risk populations, and clear diagnostic criteria remain lacking. Currently, the clinical diagnosis of epilepsy primarily depends on the patient's detailed seizure history and reliable witness accounts. Correct diagnosis facilitates the selection of optimal therapy and the evaluation of the epilepsy outcome. Mounting evidence indicates that protein glycosylation exerts specific modulatory effects on neural transmission and neural circuit excitability. Glycosylation defects often lead to central nervous system structural abnormalities, developmental delay, and seizures. With advancements in glycosylation research methods and techniques, nervous system diseases associated with glycosylation changes have garnered growing attention. This paper reviews recent studies on glycosylation changes related to epilepsy, aiming to elucidate the mechanisms of epilepsy development from a glycosylation perspective and provide a theoretical basis for epilepsy diagnosis and targeted therapy. Notably, our recently published study on kainic acid-induced epileptic rats provides direct experimental evidence for the association between abnormal glycosylation and epilepsy, further supporting the clinical relevance of glycosylation research in this field.