Search

Understanding how variations in dimensions of psychometrics, IQ and demographics relate to changes in brain connectivity during the critical developmental period of adolescence and early adulthood is a major challenge. This has particular relevance for mental health disorders where a failure to understand these links might hinder the development of better diagnostic approaches and therapeutics. Here, we investigated this question in 306 adolescents and young adults (14-24y, 25 clinically depressed) using a multivariate statistical framework, based on canonical correlation analysis (CCA). By linking individual functional brain connectivity profiles to self-report questionnaires, IQ and demographic data we identified two distinct modes of covariation. The first mode mapped onto an externalization/internalization axis and showed a strong association with sex. The second mode mapped onto a well-being/distress axis independent of sex. Interestingly, both modes showed an association with age. Crucially, the changes in functional brain connectivity associated with changes in these phenotypes showed marked developmental effects. The findings point to a role for the default mode, frontoparietal and limbic networks in psychopathology and depression.

Objectives: To examine the effect of cardiovascular and metabolic diseases on initial cognitive test performance and rate of change in three cognitive measures. Design: Prospective cohort study. Setting: General practices in six towns throughout Germany. Participants: Three thousand three hundred twenty-seven participants aged 75 and older (average 79.7 ± 3.6). Measurements: Data were collected during home visits every 18 months and included sociodemographic variables, depression, disease status, drug intake, and cognition. Results: Although the presence of transient ischemic attack (TIA) or stroke and diabetes mellitus was related to poor initial cognitive test performance, the presence of those and other far-reaching chronic diseases or a higher disease burden were not related to the rate of change in cognition over time. Conclusion: Diabetes mellitus, stroke and TIA affect cognitive test performance beyond well-known sociodemographic variables and depressive symptoms, although none of these diseases contributed to cognitive decline over time. In practical terms, prevention and diagnosis of cardiovascular and metabolic diseases may be essential to cognitively healthy aging.

There is a large body of evidence showing a substantial relationship between depression and deficits in cognitive functioning. Especially in late-life depression, cognitive impairments are associated with worse treatment progress and are considered a risk factor for neurodegenerative disorders. However, little is known about the differences in neural processing and coupling during rest and cognitive functions in patients with late-life depression compared to healthy elderly individuals. The study at hand aims to investigate the cognitive control network in late-life depression during a cognitive task and at rest by means of functional near-infrared spectroscopy. Hemodynamic responses were measured at rest and during the Trail Making Test using functional near-infrared spectroscopy in a matched sample of 49 depressed and 51 nondepressed elderly subjects (age range: 51-83 years; 64.1 ± 6.58 [mean ± standard deviation]). Functional connectivity (FC) and network metrics were derived from the data and analyzed with respect to differences between the subject groups. Depressed and nondepressed subjects showed significant differences in FC both at rest and during task performance. Depressed subjects showed reduced FC in a left frontopolar cortical network during task performance and increased FC in a left frontoparietal cortical network at rest. Depressed elderly subjects showed altered FC and network organization during different mental states. Higher FC at rest may be an indicator of self-referential processes such as rumination that may reduce FC during task performance due to an overtaxed executive control system.

Objective To investigate time-dependent predictors of institutionalization in old age using a longitudinal approach. Methods In a representative survey of the German general population aged 75 years and older predictors of institutionalization were observed every 1.5 years over six waves. Conditional fixed-effects logistic regressions (with 201 individuals and 960 observations) were performed to estimate the effects of marital status, depression, dementia, and physical impairments (mobility, hearing and visual impairments) on the risk of admission to old-age home or nursing home. By exploiting the longitudinal data structure using panel econometric models, we were able to control for unobserved heterogeneity such as genetic predisposition and personality traits. Results The probability of institutionalization increased significantly with occurrence of widowhood, depression, dementia, as well as walking and hearing impairments. In particular, the occurrence of widowhood (OR = 78.3), dementia (OR = 154.1) and substantial mobility impairment (OR = 36.7) were strongly associated with institutionalization. Conclusion Findings underline the strong influence of loss of spouse as well as dementia on institutionalization. This is relevant as the number of old people (a) living alone and (b) suffering from dementia is expected to increase rapidly in the next decades. Consequently, it is supposed that the demand for institutionalization among the elderly will increase considerably. Practitioners as well as policy makers should be aware of these upcoming challenges.

Non-motor symptoms such as hyposmia and depression are often observed in Parkinson's disease (PD) and can precede the onset of motor symptoms for years. The underlying pathological alterations in the brain are not fully understood so far. Dysregulation of adult neurogenesis in the dentate gyrus of the hippocampus and the olfactory bulb has been recently suggested to be implicated in non-motor symptoms of PD. However, there is so far no direct evidence to support the relationship of non-motor symptoms and the modulation of adult neurogenesis following dopamine depletion and/or dopamine replacement. In this study, we investigated the long-term effects of l-DOPA and pramipexole, a dopamine agonist, in a mouse model of bilateral intranigral 6-OHDA lesion, in order to assess the impact of adult neurogenesis on non-motor behavior. We found that l-DOPA and pramipexole can normalize decreased neurogenesis in the hippocampal dentate gyrus and the periglomerular layer of the olfactory bulb caused by a 6-OHDA lesion. Interestingly, pramipexole showed an antidepressant and anxiolytic effect in the forced swim test and social interaction test. However, there was no significant change in learning and memory function after dopamine depletion and dopamine replacement, respectively.

At least one-third of stroke survivors suffer from depression. The development of comorbid depression after stroke is clinically highly significant because post-stroke depression is associated with increased mortality, slows recovery and leads to worse functional outcomes. Here, we review the evidence that post-stroke depression can be effectively modelled in experimental rodents via a variety of approaches. This opens an exciting new window onto the neurobiology of depression and permits probing potential underlying mechanisms such as disturbed cellular plasticity, neuroendocrine dysregulation, neuroinflammation, and neurodegeneration in a novel context. From the point of view of translational stroke research, extending the scope of experimental investigations beyond the study of short-term end points and, in particular, acute lesion size, may help improve the relevance of preclinical results to human disease. Furthermore, accumulating evidence from both clinical and experimental studies offers the tantalizing prospect of 5-hydroxytryptaminergic antidepressants as the first pharmacological therapy for stroke that would be available during the subacute and chronic phases of recovery. Interdisciplinary neuropsychiatric research will be called on to dissect the mechanisms underpinning the beneficial effects of antidepressants on stroke recovery.