Amyloid β neurotoxicity not mediated by the mitogen-activated protein kinase cascade in cultured rat hippocampal and cortical neurons
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Schisantherin A recovers Aβ-induced neurodegeneration with cognitive decline in mice
2014, Physiology and BehaviorCitation Excerpt :Evidences also suggested that the overproduction of Aβ peptides, especially Aβ1–42, oxidative stress and apoptosis induced by Aβ play a critical role in the progressive of AD [9]. It has been demonstrated that Aβ is directly toxic to cultured neurons and also induces the neurodegenerative of the CA1 region of the hippocampus, and those findings supported the hypothesis that Aβ is involved in the neurodegenerative associated with AD [10–12]. Moreover, the synthetic Aβ seemed to be responsible for neurotoxic and oxidative events leading to neurodegenerative damage in hippocampal neurons and the cultured cortical neurons [13].
Neuroprotective effects of salidroside against beta-amyloid-induced oxidative stress in SH-SY5Y human neuroblastoma cells
2010, Neurochemistry InternationalDissociation of Akt/PKB and ribosomal S6 kinase signaling markers in a transgenic mouse model of Alzheimer's disease
2008, Neurobiology of DiseaseCitation Excerpt :This result could explain the absence of modification of mTOR activation because Erk1/2 is the upstream regulator of mTOR. Other studies reported no alteration of Erk1/2 signaling in cellular models of AD (Abe and Saito, 2000; Ekinci et al., 1999). While the mTOR activation was not modified in brain of these double transgenic mice, we found a great activation of Akt, another upstream regulator of mTOR, with a robust accumulation of phosphorylated Akt at the catalytic site T308 in cytoplasm of neurons in hippocampal and cortical areas.
Cholesterol deficiency perturbs actin signaling and glutamate homeostasis in hippocampal astrocytes
2006, Brain ResearchCitation Excerpt :As noted, the enhanced activation of ERK occurs in an astrocyte-specific manner. This is reminiscent of the finding that Aβ caused ERK activation in astrocytes, but not in neurons (Abe and Saito, 2000b). Abe and Saito previously reported that activation of Glu transporter led to phosphorylation of ERK in astrocytes (Abe and Saito, 2001).
Decreased phosphorylation and protein expression of ERK1/2 in the brain of hypoxic preconditioned mice
2006, Neuroscience Letters