The two parallel pathways are discussed, as well as their implications for the catalytic cycle of this enzyme.”
“SCOP (suprachiasmatic nucleus (SCN) circadian oscillatory protein) was originally identified in 1999 in a differential display screen of the rat SCN for genes whose expression were regulated in a circadian manner (K. Shimizu, A-1210477 M. Okada, A. Takano and K. Nagai, FEBS Lett., 1999, 458, 363-369). The SCN is the principle pacemaker of the

circadian clock, and expression of SCOP protein in the SCN was found to oscillate, increasing during the subjective night, even when animals were housed in constant darkness. SCOP interacts with and inhibits multiple proteins important for intracellular signaling, either by directly binding to K-Ras or by dephosphorylating p-Akt and p-PKC. Since

the functions of K-Ras, Akt, and PKC are considerably divergent, SCOP may have several roles. We recently discovered that SCOP participates in the formation of long-term hippocampus-dependent memories, and other investigators selleck screening library have examined its role in cell proliferation and survival. In this review, we introduce SCOP from its molecular structure to its physiological functions, focusing mainly on its role in ERK1/2 activation and memory consolidation.”
“Background: The gene encoding brain-derived neurotrophic factor (BDNF) has been suggested as a candidate for major depression, and for depression susceptibility in different neurological and psychiatric diseases. No study has investigated the role of BDNF genetic variation and depressive symptoms in Alzheimer’s disease (AD).\n\nObjective: The aim of this study was to assess the genetic contribution of BDNF Val66Met functional polymorphism to AD-related depression.\n\nMethods: Two-hundred and sixty-four AD patients underwent clinical and neuropsychological examination as well as an evaluation of behavioral and psychiatric disturbances. They were subsequently

divided into two subgroups according to the BI 2536 clinical trial presence (AD-D) or the absence (AD-nD), based on DSM-IV criteria for depression in AD. In each subject, BDNF Val66Met functional polymorphism and apolipoprotein E (APOE) genotype were evaluated.\n\nResults: In our sample, 35.2% of patients (n = 93) reported AD-related depressive symptoms. Compared to patients bearing no polymorphisms (BDNF GIG), BDNF G/A carriers showed more than twofold-time risk (OR = 2.38; 95%CI = 1.38-4.13), and BDNF A/A carriers had a threefold-time risk (OR = 3.04; 95%CI = 1.15-8.00) for depression in AD.\n\nAccordingly, considering the allele frequencies, BDNF A allele was significantly over-represented in AD-D (32.8%) compared to AD-nD (19.0%) (OR = 2.08; 95%CI = 1.38-3.13). An association between the number of carried A allele and the severity of depressive symptoms was observed (P < 0.002). No effect of APOE genotype on risk for depression was found.