Isoproterenol, an adrenergic β receptor agonist, induces metallothionein synthesis followed by canceling amyloid β1-42-induced neurodegeneration

A PAM of the α1A-Adrenergic receptor rescues biomarker, long-term potentiation, and cognitive deficits in Alzheimer’s disease mouse models without effects on blood pressure

“…Similarly, α 2A -AR agonists which inhibit NE release from sympathetic nerve endings also increase amyloidogenesis and plaque burden ( Chen et al, 2014 ). β 2 -AR activation is neuroprotective against amyloid toxicity ( Tamano et al, 2018 ; Kawano et al, 2022 ; Chai et al, 2022 ). There are no prior reports concerning effects of α 1 -ARs in amyloid biology.…”

Metallothionein synthesis increased by Ninjin-yoei-to, a Kampo medicine protects neuronal death and memory loss after exposure to amyloid β1-42

“…Exogenous catecholamines including isoproterenol, which cannot pass through the blood–brain barrier, induces MTs in peripheral tissues, e.g., the liver and kidney [ 23 – 25 ]. Isoproterenol, an adrenergic β receptor agonist, enhances MT synthesis in the dentate gyrus and cancels neurodegeneration via intracellular Zn 2+ toxicity after ICV co-injection of Aβ 1-42 and isoproterenol [ 26 ]. It is estimated that MT synthesis is enhanced by adrenergic β receptor-mediated signaling after the intake of NYT diet and contributes to ameliorating Aβ 1-42 toxicity in the brain.…”