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Our previous studies have confirmed that the activation of NgR on microglia by Nogo promotes the expression of proinflammatory cytokines and inhibits cell adhesion and migration behaviors. These results contribute to a better understanding of AD pathogenesis and could offer a new therapeutic option for delaying the progression of AD.
The online version of this article More than 24 million people are affected in the world [ 2 ]. Nogo-A is a myelin-associated inhibitory molecule that inhibits the growth of neurite and reconnection in CNS diseases through cellar and molecular events [ 3 , 4 ]. Nogo receptor NgR is a glycosylphosphatidylinositol-linked receptor, which binds with high affinity to Nogo, a hydrophilic 66 amino acid-long region of Nogo-A [ 5 ].
Recently, a number of studies have suggested that Nogo and its receptor participate in the AD pathogenesis. For example, it has been demonstrated that the expression of Nogo-A is increased in the hippocampus of patients with AD and is also localized in senile plaques around amyloid deposits [ 6 ].