The neuroprotective effect and mechanisms Elafibranor of NRG1 in SH-SY5Y cells over-expressing the Swedish mutant form of amyloid precursor protein (Swe-APP) and primary cortical neuronal

cells treated with amyloid beta peptide(1-42) (A beta(1-42)) were investigated in this study. NRG1 attenuated Swe-APP- or A beta(1-42)-induced lactate dehydrogenase (LDH) release in a concentration-dependent manner. The mitigating effects of NRG1 on neuronal cell death were blocked by ErbB4 inhibition, a key NRG1 receptor, which suggests a role of ErbB4 in the neuroprotective function of NRG1. Moreover, NRG1 reduced the number of Swe-APP- and A beta(1-42)-induced TUNEL-positive SH-SY5Y cells and primary cortical neurons, respectively. NRG1 reduced the accumulation of reactive oxygen species and attenuated Swe-APP-induced mitochondrial membrane potential loss. NRG1 also induced the upregulation of the expression of the anti-apoptotic protein, Gemcitabine in vivo Bcl-2, and decreased caspase-3 activation. Collectively, our results demonstrate that NRG1 exerts neuroprotective effects via the ErbB4 receptor, which suggests the neuroprotective potential of NRG1 in AD. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Objective: To determine a) whether clinical response to electroconvulsive therapy (ECT) is associated with decreased platelet activation in patients with major depressive disorder (MDD) and b) if any medical/demographic characteristics

predict response to ECT or changes in platelet activation. Increased platelet activation may underlie the increased risk of coronary buy LB-100 artery disease (CAD) in patients with MDD. Methods: Before their first

and sixth ECT treatments, study patients (n = 44) completed the Beck Depression Inventory (BDI) to assess the severity of depressive symptoms. Activity of the platelet thromboxane (TBX) A(2) pathway was assessed by measuring the morning spot urinary concentrations of 11-dehydroxy-thromboxane B-2 (11-D-TBX 132), a major metabolite of plate let-derived TBX A(2). Results: Multivariate logistic regression analyses revealed that improvement on the BDI was significantly more likely in patients without a history of hypertension (p = .02) and in patients who were prescribed a greater number of “”plate let-altering”" medications (p = .03). During a course of ECT, a decrease in urinary 11-D-TBX B-2 was significantly more likely to occur in ECT nonresponders (p = .01) and younger patients (p = .02). Conclusions: Clinical response to ECT coadministered may not be associated with decreases in platelet-derived TBX. Future studies will confirm which somatic “”antidepression”" treatments offer optimal thrombovascular benefits for depressed patients with multiple risk factors for, or clinically evident, cerebral disease or CAD.”
“Ionotropic receptors mediate rapid communication between neurons. These receptors are oligomers and are usually assembled from multiple subunit types.