Topic: Kir4.1

Healthy brain activity relies on the presence of key astrocytic proteins: the excitatory amino acid transporters (EAAT1/2), inwardly rectifying K+ channel (Kir4.1), aquaporin-4 (AQP4) among others. In the aging cortex, we report a novel phenotype of individual, sparse, non-reactive astrocytes with unchanged morphology, but greatly reduced levels of EAATs, Kir4.1, AQP4, and other astrocytic proteins, while bordering cells retain robust immunolabeling. Astrocyte tiling remains intact leaving these domains without many essential astrocytic functions. Already documented in a concussive mouse model

Immune recognition of non-self or self proteins may be either favored or hampered by antigen posttranslational modifications such as citrullination, phosphorylation or N-glycosylation. This may contribute to autoimmunity such as in multiple sclerosis (MS), a demyelinating CNS disorder. Strikingly, the glial potassium channel KCNJ10 (Kir4.1) can exhibit low to high glycosylated forms and initial works from different laboratories identified variable proportions of MS patients harboring high levels of anti-Kir4.1 IgGs. Using a well-controlled ELISA, six percent of MS patients exhibit high seric l