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Readthrough isoform of aquaporin-4 (AQP4) as a therapeutic target for Alzheimer’s disease and other proteinopathies

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  • معلومة اضافية
    • Contributors:
      Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB); Centre Hospitalier Régional Universitaire Montpellier (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM); Institut des Neurosciences de Montpellier (INM); Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM); Laboratoire de biologie physico-chimique des protéines membranaires (LBPC-PM (UMR_7099)); Institut de biologie physico-chimique (IBPC (FR_550)); Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité); CHU Montpellier; Centre Hospitalier Régional Universitaire Montpellier (CHRU Montpellier)
    • بيانات النشر:
      HAL CCSD
      BioMed Central
    • الموضوع:
      2023
    • Collection:
      Inserm: HAL (Institut national de la santé et de la recherche médicale)
    • نبذة مختصرة :
      International audience ; The glymphatic system is a crucial component in preserving brain homeostasis by facilitating waste clearance from the central nervous system (CNS). Aquaporin-4 (AQP4) water channels facilitate the continuous interchange between cerebrospinal fluid and brain interstitial fluid by convective flow movement. This flow is responsible for guiding proteins and metabolites away from the CNS. Proteinopathies are neurological conditions characterized by the accumulation of aggregated proteins or peptides in the brain. In Alzheimer’s disease (AD), the deposition of amyloid-β (Aβ) peptides causes the formation of senile plaques. This accumulation has been hypothesized to be a result of the imbalance between Aβ production and clearance. Recent studies have shown that an extended form of AQP4 increases Aβ clearance from the brain. In this mini-review, we present a summary of these findings and explore the potential for future therapeutic strategies aiming to boost waste clearance in AD.
    • Relation:
      info:eu-repo/semantics/altIdentifier/pmid/37821965; hal-04649689; https://hal.science/hal-04649689; https://hal.science/hal-04649689/document; https://hal.science/hal-04649689/file/s13195-023-01318-2.pdf; PUBMED: 37821965; PUBMEDCENTRAL: PMC10566184; WOS: 001082076200001
    • الرقم المعرف:
      10.1186/s13195-023-01318-2
    • الدخول الالكتروني :
      https://hal.science/hal-04649689
      https://hal.science/hal-04649689/document
      https://hal.science/hal-04649689/file/s13195-023-01318-2.pdf
      https://doi.org/10.1186/s13195-023-01318-2
    • Rights:
      http://creativecommons.org/licenses/by/ ; info:eu-repo/semantics/OpenAccess
    • الرقم المعرف:
      edsbas.20A09BF6