Conclusion The results of our study suggest that specific psychopathological features in depression may be linked to 5-HT and/or NA dysfunction. Future studies should evaluate whether these findings may be relevant for the selection of antidepressant strategies. However, the fact that 40% of major depressed inpatients do not showabnormalities of NA and/ or 5-HT system responsiveness, and that NA and/or 5-HT dysfunction are not associated with the core of depressive

symptoms, support the view that NA and/or 5-HT dysfunction Inhibitors,research,lifescience,medical is less likely to be the primary cause of mood disorders47 , 48 but is more indicative of failure of compensatory mechanisms involved in affective homeostasic processes. Selected abbreviations and acronyms CLO clonidine FCA factorial carrespondence analysis d-FEN d-fenfluramine GH growth hormone 5-HT serotonin NA naradrenaline PRL prolactin Notes We would like to thank Inhibitors,research,lifescience,medical the nursing staff of sector VIII and Gabrielle Wagner, pharmacist, for performing the hormone analysis.
Alzheimer’s disease (AD) is the most common cause of dementia in the elderly, accounting for up to 70% of all cases.1 Many potential causes

of neuronal injury in AD have been Inhibitors,research,lifescience,medical identified, including neurotoxic effects of the beta-amyloid peptide (β-AP),2 hyperphosphorylation of microtubule-associated protein tau,3 the effects of the apolipoprotein E4 isoform,4 and expression of mutant presenilin proteins.5 In addition, there is a chronic inflammatory

response Inhibitors,research,lifescience,medical in the AD brain that has recently received increased attention as a potential cause of neuronal injury in AD, and as a potential therapeutic target. This paper will review the evidence for inflammatory injury to neurons in AD, focusing Inhibitors,research,lifescience,medical particularly on the role of Selleck GW-572016 microglial cells. Cerebral inflammation in AD: microglial cells and β-AP According to the inflammatory hypothesis of AD, chronic cerebral inflammation results in injury to neurons, contributing over time to cognitive decline. Neuronal injury is hypothesized to result from the direct effects of inflammatory effectors, such as cytokines Metalloexopeptidase or activated complement, or indirect effects, such as increased production of neurotoxic β-AP in response to cytokines or other inflammatory stimuli.6,7 Originally based on the presence of markers for inflammation in and around neuritic plaques,8,9 this hypothesis has generated a large volume of in vitro cellular and molecular data indicating a variety of possible mechanisms for inflammatory injury to the AD brain. Further, a number of epidemiologic studies indicate that anti-inflammatory medications may protect against AD.