a(MESH:"Cholinesterase Inhibitors")
Likewise, blocking the PI3K-AKT pathway inhibits the protective effects of AChE inhibitors on neuroblastoma cells or neuronal cells against Abeta (Arias et al., 2005) or L-glutamate neurotoxicity (Takada-Takatori et al., 2006). In all these studies, protection was also inhibited by nAChR blockers, suggesting that these effects are mediated by nAChRs. PubMed:19293145
Several lines of evidence point to a link between brain nAChRs and the development of AD. Biochemical analysis of brains of patients with AD reveals deficits in nAChRs, an increase in butyrylcholinesterase, reduction in ACh, and attenuated activity of cholinergic synthetic [choline acetyltransferase (ChAT)] and inactivating (AChE) enzymes (Bartus et al., 1982; Francis et al., 1999).Butyrylcholinesterase and AChE help terminate ACh signaling by hydrolyzing the transmitter, thereby inactivating it. PubMed:19293145
In fact, as described above, AChE inhibitors do not affect alpha7 nAChR-mediated synaptic transmission evoked by low-frequency stimulation of cholinergic fibers in chick ciliary ganglia (522). PubMed:19126755
Likewise, blocking the PI3K-AKT pathway inhibits the protective effects of AChE inhibitors on neuroblastoma cells or neuronal cells against Abeta (Arias et al., 2005) or L-glutamate neurotoxicity (Takada-Takatori et al., 2006). In all these studies, protection was also inhibited by nAChR blockers, suggesting that these effects are mediated by nAChRs. PubMed:19293145
Likewise, blocking the PI3K-AKT pathway inhibits the protective effects of AChE inhibitors on neuroblastoma cells or neuronal cells against Abeta (Arias et al., 2005) or L-glutamate neurotoxicity (Takada-Takatori et al., 2006). In all these studies, protection was also inhibited by nAChR blockers, suggesting that these effects are mediated by nAChRs. PubMed:19293145
Cholinesterase inhibitors can increase ACh levels in the synaptic cleft and partially ameliorate cognitive symptoms, enhance quality of life and diminish caregiver burden for patients with mild to severe AD PubMed:26813123
Cholinesterase inhibitors can increase ACh levels in the synaptic cleft and partially ameliorate cognitive symptoms, enhance quality of life and diminish caregiver burden for patients with mild to severe AD PubMed:26813123
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