https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34716 Wed 15 Dec 2021 16:10:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12136 Wed 11 Apr 2018 15:30:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30351 1 or CGRP₂ receptor in which it demonstrates similar high-affinity binding for salmon calcitonin, CGRP, and amylin, a possession which is not shared by any extra CGRP receptors. Binding of CGRP to its receptor increases activated cAMP-dependent pkA and PI3 kinase, resulting in N-terminal fragments that are shown to exert complex inhibitory as well facilitator actions on nAChRs. Fragments such as CGRP1-4, CGRP1-5, and CGRP1-6 rapidly as well as reversibly improve agonist sensitivity of nAChRs without straight stimulating those receptors and produce the Ca²⁺-induced intracellular Ca²⁺ mobilization. Renin–angiotensin–aldosterone system (RAAS)-activated angiotensin-type (AT4) receptor is also beneficial in AD. It has been suggested that exogenous administration of CGRP inhibits infiltration of macrophages and expression of various inflammatory mediators such as NFkB, IL-1b, TNF-α, iNOS, matrix metalloproteinase (MMP)-9, and cell adhesion molecules like intercellular adhesion molecule (ICAM)-1 which attenuates consequence of inflammation in AD. Donepezil, a ChEI, inhibits acetylcholinesterase and produces angiogenesis and neurogenesis, in the dentate gyrus of the hippocampus of WT mice after donepezil administration. However, none of the results discovered in CGRP-knockout mice and WT mice exposed to practical denervation. Therefore, selective agonists of CGRP receptors may become the potential candidates for treatment of AD]]> Wed 10 Nov 2021 15:13:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27891 Mon 23 Sep 2019 10:12:42 AEST ]]>