“…Moreover, activation of Cdks can be triggered in brain neurons after cerebral ischemia or kainate-induced excitotoxicity as well as in cultured neurons after treatment with DNAdamaging agents, deprivation of toxic factors, or -amyloid peptide (Park et al 1997a(Park et al ,b, 1998a(Park et al ,b, 2000Copani et al, 1999;Stefanis et al, 1999;Osuga et al, 2000;Ino and Chiba, 2001;Katchanov et al, 2001). Under such in vivo and in vitro conditions, neuronal death can be rescued by the use of Cdk inhibitors or dominant negative forms of the kinases (Park et al 1997a(Park et al ,b, 1998a(Park et al ,b, 2000Copani et al, 1999;Stefanis et al, 1999;Osuga et al, 2000;Ino and Chiba, 2001;Katchanov et al, 2001), demonstrating the central role of Cdks in the neuronal apoptotic mechanism (for review, see Nguyen et al, 2002b).…”