Topic: aquaporin-4

Glymphatic perivascular exchange is supported by the astroglial water channel aquaporin-4 (AQP4), which localizes to perivascular astrocytic endfeet surrounding the cerebral vasculature. In aging mice, impairment of glymphatic function is associated with reduced perivascular AQP4 localization, yet whether these changes contribute to the development of neurodegenerative disease, such as Alzheimer’s disease (AD), remains unknown. Using post mortem human tissue, we evaluated perivascular AQP4 localization in the frontal cortical gray matter, white matter, and hippocampus of cognitively normal sub

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

Neuromyelitis-optica spectrum disorders (NMOSD) usually associate with aquaporin-4 (AQP4) or myelin oligodendrocyte glycoprotein (MOG) antibodies. Seronegative-NMOSD (SN-NMOSD) has been described, but the clinical-therapeutic profile is poorly defined.We searched PubMed, Scopus and Google Scholar databases for studies reporting SN-NMOSD patients, on which anti-MOG-Abs and AQP4-Abs were tested. PRISMA guidelines and methodological quality control were assessed. Fixed or random-effects models were used to pool results across studies.We included 36/1027 articles screened and analyzed 591 SN-NMOSD

Atypical astrocytes (AtAs) are a distinct subset of non-reactive astrocytes in the brain characterized by dramatically diminished expression of excitatory amino acid transporters (GLAST, GLT1) and other astrocytic proteins. Our ongoing research on the development and progression of AtAs in naïve wild type (WT) mice has shown significant regional and age effects. We have also shown that brain tissue from confirmed Alzheimer’s Disease (AD) patients, as well as healthy controls, have areas of presumptive AtAs. This study aims to further explore the role of AtAs in AD pathology utilizing the APPNL