Amyloid and Tau as cerebrospinal fluid biomarkers in anti-N-Methyl-D-aspartate receptor encephalitis.

INTRODUCTION: Neuroinfection is associated with the deposition of amyloid-beta (Aβ) peptides, and subsequent decrease in cerebrospinal fluid (CSF) amyloid levels. However, whether autoimmune encephalitis involves extracellular deposition of Aβ peptides in the brain is unreported.

METHODS: We examined CSF amyloid and tau values in adults with anti-N-methyl-D-aspartate receptor encephalitis (NMDAR-E). Forty-two patients with NMDAR-E, 35 patients with viral and bacterial neuroinfections, and 16 controls were included. We measured CSF Aβ1-42 (cAβ1-42), Aβ1-40 (cAβ1-40), t-Tau (ct-Tau), and p-Tau181 (cp-Tau181) levels and assessed their efficacies regarding differential diagnosis and predicting prognosis.

RESULTS: NMDAR-E patients had lower cAβ1-42 levels; however, they were higher than those of patients with bacterial meningitis. ct-Tau levels in NMDAR-E patients were lower than those in patients with neuroinfections. No changes were observed in controls. cAβ1-42 and ct-Tau were combined as an excellent marker to distinguish NMDAR-E from neuroinfections. cAβ1-42 levels in NMDAR-E patients were positively correlated with Montreal Cognitive Assessment scores. We observed an inverse relationship between cAβ1-42 levels and modified Rankin Scale scores. Patients with poor outcomes exhibited low cAβ1-42 levels and high levels of several blood parameters. cAβ1-42 was the highest quality biomarker for assessing NMDAR-E prognosis. Correlations were found between cAβ1-42 and some inflammatory indicators.

CONCLUSION: cAβ1-42 was decreased in NMDAR-E patients. cAβ1-42 levels indicated NMDAR-E severity and acted as a biomarker for its prognosis. Combining cAβ1-42 and ct-Tau levels could serve as a novel differential diagnostic marker for NMDAR-E.