
Uncovering a New Aβ Receptor: A Key to Controlling Neuronal Hyperactivity in Alzheimer’s Disease
No se pudo agregar al carrito
Add to Cart failed.
Error al Agregar a Lista de Deseos.
Error al eliminar de la lista de deseos.
Error al añadir a tu biblioteca
Error al seguir el podcast
Error al dejar de seguir el podcast
-
Narrado por:
-
De:
Acerca de esta escucha
In this episode of the Journal of Neurophysiology's podcast series, we spotlight the research titled “Discovery of the Aβ receptor that controls the voltage-gated sodium channel activity: unraveling mechanisms underlying neuronal hyperexcitability.”
Alzheimer’s disease is well known for memory loss and cognitive decline—but behind these symptoms lies a web of complex neuronal dysfunction. This study reveals that amyloid beta peptides (Aβs), known to enhance sodium channel activity and drive hyperexcitability, exert their effects via an unexpected molecular player: the type I taste receptor, T1R2/T1R3.
Using advanced patch-clamp techniques, the researchers identified this novel Aβ receptor, opening a promising new path for therapeutic intervention. By targeting this receptor, future treatments may be able to reduce Aβ-induced hyperactivity and slow AD progression.
Discovery of the Aβ receptor that controls the voltage-gated sodium channel activity: unraveling mechanisms underlying neuronal hyperexcitability Mitsuyoshi Luke Saito, Tsutomu Sasaki, and Mariko Ruth Saito
Journal of Neurophysiology 2025 133:6, 1861-1885