Ayşit Altuncu, NeşeUlusoy, CananÖztürk, GürkanTüzün, Erdem10.07.20192019-07-1010.07.20192019-07-102018Ayşit Altuncu, N., Ulusoy, C., Öztürk, G. ve Tüzün, E. (2018). Effect of LGI1 antibody-positive IgG on hippocampal neuron survival: A preliminary study. Neuroreport, 29(11), 932-938. https://dx.doi.org/10.1097/WNR.00000000000010550959-49651473-558Xhttps://dx.doi.org/10.1097/WNR.0000000000001055https://hdl.handle.net/20.500.12511/1979WOS: 000437757600009PubMed ID: 29771820Anti-leucine-rich glioma inactivated 1 (anti-LGI1) encephalitis is one of the most frequently encountered forms of autoimmune encephalitis. Many patients with anti-LGI1 encephalitis develop permanent hippocampal neuron loss and chronic neuropsychiatric symptoms, suggesting that LGI antibodies (Ab) might have a neurotoxic action. To investigate this hypothesis, purified serum IgG of three patients with anti-LGI1 encephalitis and six healthy controls were incubated with cultured primary hippocampal neurons obtained from newborn mice. Nontreated cells were used as controls. The viability of IgG-treated neurons was evaluated by propidium iodide staining. Apoptotic mechanisms were assessed by JC-1 assay and mRNA expression level measurement of apoptosis-related genes using real-time PCR. The effect of IgG treatment on calcium influx was analyzed by fluo-4 calcium imaging. LGI1-Ab+ IgG increased the number of propidium iodide positive neurons, reduced mitochondrial membrane potentials, upregulated caspase-3 and Bax mRNA expression levels and downregulated Bcl-2 mRNA expression levels of neurons. LGI1-Ab+ IgG-treated neurons showed lower calcium staining than healthy controls IgG-treated and non-IgG-treated neurons. Our results indicate a neurotoxic role of LGI1-Ab. This neurotoxicity is likely mediated through induction of apoptosis and reduction of calcium currents.eninfo:eu-repo/semantics/embargoedAccessAntibodyApoptosisAutoimmunityCalcium InfluxLeucine-Rich Glioma-Inactivated 1Article291193293810.1097/WNR.0000000000001055Q4Q3