Neurometabolite Concentration and Clinical Features of Chronic Alcohol Use: A Proton Magnetic Resonance Spectroscopy Study.
Neurometabolite concentration and clinical features of chronic alcohol use: A proton magnetic resonance spectroscopy study.
Filed under: Depression Treatment
Psychiatry Res. 2012 Nov 12;
Yeo RA, Thoma RJ, Gasparovic C, Monnig M, Harlaar N, Calhoun VD, Kalyanam R, Mayer AR, Durazzo TC, Hutchison KE
Chronic, heavy alcohol consumption may affect the concentration of neurometabolites assessed with proton magnetic resonance spectroscopy ((1)H-MRS). We investigated the largest sample reported to date (N=213) with the primary goal of determining how specific clinical features impact neurometabolite concentrations in an anterior cingulate gray matter voxel. This community dwelling sample included both treatment seeking and non-treatment seeking individuals. A healthy control group (N=66) was matched for age and education. In multivariate analyses predicting neurometabolite concentrations, the heavy drinking group had greater concentrations overall. An age by group interaction was noted, as group difference across neurometabolites increased with age. More years drinking, but not more drinks per drinking day (DPDD), predicted greater concentrations of choline-containing compounds (Cho), creatine-phosphocreatine (Cre), glutamate-glutamine (Glx), and n-acetyl-aspartate (NAA). The effects of other clinical variables (depression, cigarette smoking, marijuana use) were negligible. After controlling for DPDD and years drinking, treatment-seeking status had no impact on neurometabolites. In the very oldest portion of the sample (mean age=50), however, a negative relationship was seen between NAA and years drinking. These results suggest that the nature of neurometabolite abnormalities in chronic heavy drinkers may vary as a function of duration of abuse.
HubMed – depression
Brain, networks, depression, and more.
Filed under: Depression Treatment
Eur Neuropsychopharmacol. 2012 Nov 12;
Leistedt SJ, Linkowski P
Depression is a heterogeneous disorder with a highly variable course. Individual responses to treatment are inconsistent, and an established mechanism remains elusive. The classical hypothesis of depression posits that mood disorders are caused by a chemical imbalance in the brain that can be corrected with antidepressant drugs. However, recent evidence indicates that information-processing dysfunction within neural networks might underlie depression, and antidepressant drugs induce plastic changes in neuronal connectivity that gradually lead to improvements in neuronal information processing and recovery. This review presents the major current approaches to understanding the biological mechanisms of major depression, with a focus on complex brain networks.
HubMed – depression
Alzheimer’s disease pathology does not mediate the association between depressive symptoms and subsequent cognitive decline.
Filed under: Depression Treatment
Alzheimers Dement. 2012 Nov 13;
Royall DR, Palmer RF
BACKGROUND: Depressive symptoms in nondemented individuals appear to hasten the progression from mild cognitive impairment to clinical Alzheimer’s disease (AD) and double the risk of incident AD. However, the mechanism(s) by which depression might affect this risk has not been well established. The purpose of this analysis was to test the hypothesis that AD pathology mediates depression’s apparent effect on the risk of dementia conversion using longitudinally collected psychometric testing and autopsy data from the Honolulu-Asia Aging Study. METHODS: Latent factor variables representing AD, cortical Lewy body (CLB), and ischemic neuropathology were tested as potential mediators of the association between the Center for Epidemiological Studies depression scale (CES-D) score and the 10-year prospective rate of cognitive decline, adjusted for baseline cognition, age, education, total number of medications, and brain weight at autopsy. RESULTS: CES-D scores, neurofibrillary tangle counts, CLB counts, and ischemic lesions each made significant independent contributions to cognitive decline. However, CES-D scores were not significantly associated with any pathological variable; thus the pathological variables were not mediators of the effect of CES-D scores on cognitive decline. CONCLUSIONS: Subsyndromal depressive symptoms are significantly associated with subsequent cognitive decline. Although the effect is relatively modest, it is stronger than that of amyloid-related neuropathologies and independent of that of neurofibrillary tangles, cortical Lewy bodies, and ischemic lesions. Our results argue against the role of AD-related neuropathology as a mediator of depression’s effect on cognitive decline, but cannot rule out a significant mediation effect in a subset of cases, perhaps with more severe baseline depressive symptoms.
HubMed – depression
Kennedy: Jackson Jr. suffers deep depression – Patrick Kennedy talks to CNN’s Ashleigh Banfield about Jesse Jackson Jr.’s treatment for bipolar depression. For more CNN videos, check out our YouTube channel at www.youtube.com Or visit our site at www.cnn.com
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