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Ras-related protein Rab-20 (Rab20) is induced in hypoxia and contributes to hypoxia-induced apoptosis. However, the role and mechanism of Rab20 in cerebral ischemia/reperfusion (I/R) injury need to be elucidated. We established a cerebral I/R injury model in the mice and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in HT22 cells to determine the effects of Rab20 in cerebral I/R injury. Rab20 expression was upregulated in mice after I/R and in HT22 cells after OGD/R. Upregulated Rab20 was mainly located in neurons. Rab20 inhibition significantly alleviated brain infarct volume, neurological deficits, and neuronal apoptosis in mice after I/R. Moreover, Rab20 knockdown significantly ameliorated the OGD/R-induced inhibition of cell viability and apoptotic cell death in HT22 cells. Rab20 knockdown significantly alleviated OGD/R-induced mitochondrial fission by repressing mitochondrial dynamin-related protein 1 (Drp-1) recruitment and increasing Drp-1 (Ser637) phosphorylation and ameliorated mitochondrial dysfunction by reducing the mitochondrial reactive oxygen species (ROS) and cellular calcium accumulation and increasing the mitochondrial membrane potential. In addition, Rab20 knockdown significantly alleviated cytochrome c release from the mitochondria into the cytosol in HT22 cells after OGD/R. Rab20 contributes to cerebral I/R injury by regulating mitochondria-associated apoptosis pathways. Targeting Rab20 may be an attractive strategy for the treatment of cerebral I/R injury.

Abstract Background In this study, we report a case of a young female who was hospitalized for seizures and diagnosed with anti–N-methyl-D-aspartate receptor (NMDAR) encephalitis. Case presentation The main feature of this patient was bilateral temporal calcifications detected by routine head computed tomography (CT). The co-existence of anti-NMDAR encephalitis and cerebral calcifications has not been reported. We supposed that the patient had an incomplete form of celiac disease (CD), epilepsy and cerebral calcifications syndrome (CEC). The patient's symptoms were alleviated by a series of treatments, and she remained stable during the follow-ups. Conclusions Our findings confirm the rarity co-existing anti-NMDAR encephalitis and cerebral calcifications. In future clinical work, we need to elucidate the relationship between anti-NMDAR encephalitis and cerebral calcifications, and the association between anti-NMDAR encephalitis and other co-existing autoimmune disorders.

Herein, we reported a case of a young man diagnosed with MNOS (anti-myelin oligodendrocyte glycoprotein associated disease (MOGAD) and anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis overlapping syndrome, i.e., MNOS), whose imaging findings in magnetic resonance imaging (MRI) mimicked chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS). We reported a case of refractory anti-NMDAR encephalitis that recurred after standard first-line and second-line treatment. The patient presented with CLIPPERS on imaging at recent hospital admission, and his MOG antibodies were seropositive. After intravenous methylprednisolone (IVMP) treatment, the patient’s symptoms were significantly alleviated. In this case, we demonstrated that MNOS could mimic the radiological characteristics of CLIPPERS. Future studies should focus on the diagnosis and treatment of antibody overlap syndrome.