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Brain magnetic resonance imaging (MRI) performed in 2022 showed abnormal signals in bilateral upper cerebellar hemisphere, cerebellar vermis, bilateral thalamus, and bilateral hippocampus (Fig. Increased Cerebellum 18F-DPA-714 Uptake in Anti-Glutamate Kainate Receptor Subunit 2 Autoimmune Encephalitis Anti-glutamate kainate receptor subunit 2 (Gluk2) autoimmune encephalitis (AE) is a novel and very rare neuroimmune disease that was first reported in 2021.[1] Eight patients with this rare form of AE have been reported globally.[1] Herein, we report a patient with anti-Gluk2 antibodies presenting as cerebellar dysfunctions and limbic encephalitis. [Extracted from the article]

Background: Preserving the integrity of the blood-brain barrier (BBB) is beneficial to avoid further brain damage after acute ischemic stroke (AIS). Astrocytes, an important component of the BBB, promote BBB breakdown in subjects with AIS by secreting inflammatory factors. The glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 (Ex-4) protects the BBB and reduces brain inflammation from cerebral ischemia, and GLP-1R is expressed on astrocytes. However, the effect of Ex-4 on astrocytes in subjects with AIS remains unclear.Methods: In the present study, we investigated the effect of Ex-4 on astrocytes cultured under oxygen-glucose deprivation (OGD) plus reoxygenation conditions and determined whether the effect influences bEnd.3 cells. We used various methods, including permeability assays, western blotting, immunofluorescence staining, and gelatin zymography, in vitro and in vivo.Results: Ex-4 reduced OGD-induced astrocyte-derived vascular endothelial growth factor (VEGF-A), matrix metalloproteinase-9 (MMP-9), chemokine monocyte chemoattractant protein-1 (MCP-1), and chemokine C-X-C motif ligand 1 (CXCL-1). The reduction in astrocyte-derived VEGF-A and MMP-9 was related to the increased expression of tight junction proteins (TJPs) in bEnd.3 cells. Ex-4 improved neurologic deficit scores, reduced the infarct area, and ameliorated BBB breakdown as well as decreased astrocyte-derived VEGF-A, MMP-9, CXCL-1, and MCP-1 levels in ischemic brain tissues from rats subjected to middle cerebral artery occlusion. Ex-4 reduced the activation of the JAK2/STAT3 signaling pathway in astrocytes following OGD.Conclusion: Based on these findings, ischemia-induced inflammation and BBB breakdown can be improved by Ex-4 through an astrocyte-dependent manner. [ABSTRACT FROM AUTHOR]