前脑胆碱能神经元上的新型α7β2烟碱受体对Aβ敏感性的研究.pdf

A in novel，a7132-nicotinicacetyIchoIinereceptor forebrain neuronsis sensitive cholinergic highly to amyloid-betapeptides Abstract Alzheimers consideredtobethemostcommon disease(AD)is dementing， itischaracterized accumulationof disorder，and increased neurodegenerative by offorebrain neurons，and amyloidbeta(A13)peptides，degenerationcholinergic and ofthisdisorderhas learningmemorydisabilities．Althoughunderstanding advancedoverthe few mechanisms greatly past years，theprecisepathogenic remainuncertain．Anti-ADeffectsofnicotinic acetylcholine evidenceof are nAChR-mediatedattenuationofAB activity toxicity suggestedby and formation／nvitroand『仃vivo．activationofbotha—secretase amyloidplaque andAch of ofMAPK／NF啦M胁 release。facilitationApinternalization，inhibition reductionof attenuationoftau myc A13production，and signaling phosphorylation． ofnAChR on inhibition ofnAChRs Conversely，AlB-mediatedfunction，particularly forebrain bean andcriticalin neurons，couldearly stepABtoxicity cholinergic andAD forebrain neurons etiopathogenesis．Howeve