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

Adrenergic β receptor activation may ameliorate amyloid β toxicity. We examined whether isoproterenol, an adrenergic β receptor agonist reduces neurodegeneration caused by Aβ, for which intracellular Zn dysregulation is a trigger. Neurodegeneration was assessed in the dentate granule cell layer 14 days after intracerebroventricular injection of human Aβ into the mouse brain.

Preventive effect of Ninjin-yoei-to, a Kampo medicine, on amyloid β-induced neurodegeneration via intracellular Zn toxicity in the dentate gyrus.

Ninjin-yoei-to (NYT), a Kampo medicine, has ameliorative effects on cognitive dysfunction via enhancing cholinergic neuron activity. To explore an efficacy of NYT administration for prevention and cure of Alzheimer's disease, here we examined the effect of NYT on amyloid β (Aβ)-induced neurodegeneration in the dentate gyrus. A diet containing 3% NYT was administered to mice for 2 weeks and human Aβ was intracerebroventricularly injected.

Dehydroeffusol Pprevents Amyloid β-mediated Hippocampal Neurodegeneration via Reducing Intracellular Zn Toxicity.

Dehydroeffusol, a phenanthrene isolated from Juncus effusus, is a Chinese medicine. To explore an efficacy of dehydroeffusol administration for prevention and cure of Alzheimer's disease, here we examined the effect of dehydroeffusol on amyloid β (Aβ)-mediated hippocampal neurodegeneration. Dehydroeffusol (15 mg/kg body weight) was orally administered to mice once a day for 6 days and then human Aβ was injected intracerebroventricularly followed by oral administration for 12 days.

Adrenergic β receptor activation reduces amyloid β-mediated intracellular Zn toxicity in dentate granule cells followed by rescuing impairment of dentate gyrus LTP.

Adrenergic β receptor activation prevents human soluble amyloid β (Aβ)-induced impairment of long-term potentiation (LTP) in slices. On the basis of the evidence that human Aβ-induced impairment of LTP is due to Aβ-mediated Zn toxicity, we postulated that adrenergic β receptor activation reduces Aβ-mediated intracellular Zn toxicity followed by rescuing Aβ toxicity. To test the effect of adrenergic β receptor activation, LTP was recorded at perforant pathway-dentate granule cell synapses of anesthetized rats 60 min after Aβ injection into the dentate granule cell layer.