"3"^^ . "Psychiatrie" . . "Alzheimer's disease; muscarinic acetylcholine receptors; agonists of M1 subtype receptor; AF267B"@en . . . . . . . "Remarkable molecule AF267B and Alzheimer's disease"@en . "CZ - \u010Cesk\u00E1 republika" . . "Remarkable molecule AF267B and Alzheimer's disease"@en . "Pozoruhodn\u00E1 molekula AF267B a Alzheimerova nemoc"@cs . . "4" . . "Pato\u010Dka, Ji\u0159\u00ED" . . . "Pozoruhodn\u00E1 molekula AF267B a Alzheimerova nemoc" . "[95BF18C9185D]" . . "1211-7579" . "Pozoruhodn\u00E1 molekula AF267B a Alzheimerova nemoc" . "Alzheimerova nemoc (AD) p\u0159edstavuje nej\u010Dast\u011Bj\u0161\u00ED neurodegenerativn\u00ED onemocn\u011Bn\u00ED st\u0159edn\u00EDho a pozd\u011Bj\u0161\u00EDho v\u011Bku. lavn\u00EDm rysem AD je cholinergn\u00ED deficit, proto inhibitory cholinester\u00E1zy \u0159edstavuj\u00ED jeden z nejv\u00FDznamn\u011Bj\u0161\u00EDch prost\u0159edk\u016F ke zm\u00EDrn\u011Bn\u00ED t\u00E9to dysfunkce. Inhibitory cholinester\u00E1zy poskytuj\u00ED m\u00EDrnou symptomatickou \u00FAlevu, ale jejich \u00FA\u010Dinnost se \u010Dasem sni\u017Euje, proto\u017Ee nejsou schopny l\u00E9\u010Dit z\u00E1kladn\u00ED principy nemoci. Alternativn\u00ED strategie obnoven\u00ED cholinergn\u00EDch funkc\u00ED a zm\u00EDrn\u011Bn\u00ED \u00FAbytku kognitivn\u00EDch funkc\u00ED spo\u010D\u00EDv\u00E1 v p\u016Fsoben\u00ED na receptory, na nich\u017E acetylcholin funguje jako neuromedi\u00E1tor. Stimulace muskarinov\u00FDch acetylcholinov\u00FDch receptor\u016F, zejm\u00E9na podtypu M1, prok\u00E1zala p\u0159\u00EDzniv\u00FD vliv na obnoven\u00ED kognitivn\u00EDch funkc\u00ED u pacient\u016F s AD a na \u00FAtlum tvorby Abeta a tau proteinu v r\u016Fzn\u00FDch zv\u00ED\u0159ec\u00EDch modelech. Bylo ji\u017E testov\u00E1no n\u011Bkolik centr\u00E1ln\u011B p\u016Fsob\u00EDc\u00EDch muskarinov\u00FDch agonist\u016F. Jeden z nich, AF267B, tak\u00E9 prok\u00E1zal schopnost zabr\u00E1nit kognitivn\u00EDmu deficitu v modelech Alzheimerovy choroby. V tomto \u010Dl\u00E1nku je diskutov\u00E1na mo"@cs . . "Pozoruhodn\u00E1 molekula AF267B a Alzheimerova nemoc"@cs . "Alzheimer's disease (AD) represents the most common neurodegenerative disease occurring in mid-to-late life. Cholinergic deficit is a cardinal feature of AD, and cholinesterase inhibitors represent one of the most prominent means of mitigating this dysfunction. Cholinesterase inhibitors provide mild symptomatic relief, although they lose their efficacy over time most likely because they are not disease-modifying agents. An alternative strategy for restoring cholinergic function and attenuating the cognitive decline involves acting on the receptors on which acetylcholine acts. Stimulation of muscarinic acetylcholine receptors and in particular the M1 subtype has been shown to have a beneficial effect in restoring cognition in patients with Alzheimer's disease and in attenuating Abeta and tau pathology in different animal models. Several centrally active muscarinic agonists were tested. One of them, compound AF267B, can also rescue selected deficits in Alzheimer's models. In this article,"@en . "2"^^ . . "RIV/60076658:12110/10:00012127" . "1"^^ . "Alzheimerova nemoc (AD) p\u0159edstavuje nej\u010Dast\u011Bj\u0161\u00ED neurodegenerativn\u00ED onemocn\u011Bn\u00ED st\u0159edn\u00EDho a pozd\u011Bj\u0161\u00EDho v\u011Bku. lavn\u00EDm rysem AD je cholinergn\u00ED deficit, proto inhibitory cholinester\u00E1zy \u0159edstavuj\u00ED jeden z nejv\u00FDznamn\u011Bj\u0161\u00EDch prost\u0159edk\u016F ke zm\u00EDrn\u011Bn\u00ED t\u00E9to dysfunkce. Inhibitory cholinester\u00E1zy poskytuj\u00ED m\u00EDrnou symptomatickou \u00FAlevu, ale jejich \u00FA\u010Dinnost se \u010Dasem sni\u017Euje, proto\u017Ee nejsou schopny l\u00E9\u010Dit z\u00E1kladn\u00ED principy nemoci. Alternativn\u00ED strategie obnoven\u00ED cholinergn\u00EDch funkc\u00ED a zm\u00EDrn\u011Bn\u00ED \u00FAbytku kognitivn\u00EDch funkc\u00ED spo\u010D\u00EDv\u00E1 v p\u016Fsoben\u00ED na receptory, na nich\u017E acetylcholin funguje jako neuromedi\u00E1tor. Stimulace muskarinov\u00FDch acetylcholinov\u00FDch receptor\u016F, zejm\u00E9na podtypu M1, prok\u00E1zala p\u0159\u00EDzniv\u00FD vliv na obnoven\u00ED kognitivn\u00EDch funkc\u00ED u pacient\u016F s AD a na \u00FAtlum tvorby Abeta a tau proteinu v r\u016Fzn\u00FDch zv\u00ED\u0159ec\u00EDch modelech. Bylo ji\u017E testov\u00E1no n\u011Bkolik centr\u00E1ln\u011B p\u016Fsob\u00EDc\u00EDch muskarinov\u00FDch agonist\u016F. Jeden z nich, AF267B, tak\u00E9 prok\u00E1zal schopnost zabr\u00E1nit kognitivn\u00EDmu deficitu v modelech Alzheimerovy choroby. V tomto \u010Dl\u00E1nku je diskutov\u00E1na mo" . "Ku\u010Da, Kamil" . "12110" . . "V, Z(MO0FVZ0000604)" . "RIV/60076658:12110/10:00012127!RIV11-MSM-12110___" . "14" . . "280733" .