Acetylcholinesterase inhibitors used in treatment of Alzheimer's disease prevent glutamate neurotoxicity via nicotinic acetylcholine receptors and phosphatidylinositol 3-kinase cascade

@article{TakadaTakatori2006AcetylcholinesteraseIU,
  title={Acetylcholinesterase inhibitors used in treatment of Alzheimer's disease prevent glutamate neurotoxicity via nicotinic acetylcholine receptors and phosphatidylinositol 3-kinase cascade},
  author={Yuki Takada-Takatori and Toshiaki Kume and Mitsuhiro Sugimoto and Hiroshi Katsuki and Hachiro Sugimoto and Akinori Akaike},
  journal={Neuropharmacology},
  year={2006},
  volume={51},
  pages={474-486}
}

Roles of nicotinic receptors in acetylcholinesterase inhibitor-induced neuroprotection and nicotinic receptor up-regulation.

It is shown that acetylcholinesterase inhibitors protect neurons from glutamate-induced neurotoxicity in the primary culture of rat cortical neurons and that nicotinic receptor expression levels are regulated, a property which may have some bearing on their therapeutic effects.

Mechanisms of Neuroprotective Effects of Nicotine and Acetylcholinesterase Inhibitors: Role of α4 and α7 Receptors in Neuroprotection

Results suggest that nicotine as well as AChE inhibitors, donepezil and galantamine, prevent glutamate neurotoxicity through α4 and α7 nAChRs and the PI3K-Akt pathway.

Acetylcholinesterase inhibitors rapidly activate Trk neurotrophin receptors in the mouse hippocampus

Nicotinic Acetylcholine Receptor Signaling: Roles in Neuroprotection

Results suggest that nAChR stimulation suppresses the inflammatory response induced by bradykinin via the PI3K-Akt pathway in astrocytes, and suggests that nicotine as well as donepezil prevents glutamate neurotoxicity through Α4- and α7-nAChRs and the phosphatidylinositol 3-kinase (PI3K)/Akt pathways.

Donepezil, a potent acetylcholinesterase inhibitor, induces caspase-dependent apoptosis in human promyelocytic leukemia HL-60 cells.

It is demonstrated for the first time that donepezil displayed an induction of apoptosis in HL-60 cells via a mitochondria-mediated caspase-dependent pathway.
...

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