1,293 publications from this institution
There is evidence that immune-inflammatory, stress of reactive oxygen and nitrogen species (IO&NS) processes play a role in the neurodegenerative processes observed in Parkinson's disease (PD). The aim of the present study was to investigate peripheral IO&NS biomarkers in PD. We included 56 healthy individuals and 56 PD patients divided in two groups: early PD stage and late PD stage. Plasma lipid hydroperoxides (LOOH), malondialdehyde (MDA), nitric oxide metabolites (NOx), sulfhydryl (SH) groups, catalase (CAT) activity, superoxide dismutase (SOD) activity, paraoxonase (PON)1 activity, total radical trapping antioxidant parameter (TRAP) and C-reactive protein (CRP) were measured. PD is characterized by increased LOOH, MDA and SOD activity and lowered CAT activity. A combination of five O&NS biomarkers highly significantly predicts PD with a sensitivity of 94.5% and a specificity of 86.8% (i.e., MDA, SOD activity, TRAP, SH-groups and CAT activity). The single best biomarker of PD is MDA, while LOOH and SOD activity are significantly associated with late PD stage, but not early PD stage. Antiparkinson drugs did not affect O&NS biomarkers, but levodopa+carbidopa significantly increased CRP. It is suggested that MDA may serve as a disease biomarker, while LOOH and SOD activity are associated with late PD stage characteristic. New treatments for PD should not only target dopamine but also lipid peroxidation.
L-tryptophan (L-TRP), the competing amino acids (CAA) valine and leucine and the cortisol levels taken at 8 a.m. after administration of dexamethasone on the previous day, were determined in 160 patients suffering from depression. The ratio between the L-TRP values and the sum of the competing amino acids was calculated. The clinical relevance of the L-TRP/CAA ratio in the case of major depression (DSM-III) versus minor depression (dysthymic disorder, atypical depression and adaptation disorder with depressive mood) was studied in comparison with the DST. Patients suffering from major depression showed a significantly decreased (p = 0.0006) L-TRP/CAA ratio. The combination of a decreased L-TRP/CAA ratio (cut off point less than or equal to 0.130) or an abnormal DST (cut off point greater than or equal to 3.5 micrograms/dl) is the best criterion which allows 59.0% of the patients suffering from major depression to be identified correctly with a specificity of 90.9%; the above-mentioned criterion permits 70.0% of the patients to be classified correctly into their actual group.
Synopsis The widely applied procedure of balancing self-report instruments by including positively and negatively keyed items is exemplified by the Zung Self-rating Depression Scale (SDS). Investigation of the influence of the symptom-positive and symptom-negative item modes on the SDS in a depressed population resulted in two major findings. First, the reversed scoring of the symptom-negative items resulted in higher mean item scores. Secondly, factor analyses of the SDS in the present study and in previous research revealed that the semantic modes of item presentation were represented in the factor structure of the SDS. These findings were confirmed by analyses with the State–Trait Anxiety Inventory (STAI) and by previous factor analytical research with balanced instruments and were interpreted within the framework of the theory of Positive and Negative Affect. The present data cast doubts on the construct validity of the SDS as a measure of depressive symptomatology due to the presence of the negatively keyed items and suggest reconsideration of the use of balanced instruments for minimization of the acquiescence response set.
It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.
This study investigates the utility for depression research of an assay for intact (1–39) adrenocorticotropic hormone (ACTH) versus that of a previously employed (i.e., 1–17, 1–24 sequences) ACTH assay. ACTH plasma levels were measured using two different ACTH assays (labeled as intact versus nonintact) in 10 minor and 27 major depressed subjects undergoing the combined dexamethasone suppression (DST) and corticotropin-releasing hormone (CRH) test. Intact – but not nonintact – ACTH values were significantly correlated with the severity of illness. Major depressed subjects exhibited significantly higher post-DST+CRH intact ACTH values than minor depressives, whereas nonintact ACTH values were not significantly different between these groups. Post-DST+CRH intact ACTH values were significantly more closely related to post-DST+CRH cortisol than nonintact ACTH values. It is concluded that the assay of the intact ACTH molecule is an asset in depression research and should replace the previous less specific and sensitive ACTH assays.
