Persistence of neuropsychologic deficits in the remitted state of late-life depression.
ABSTRACT Cognitive impairment in late-life depression (LLD) is prevalent, disabling, and persists despite the remission of depressive symptoms. This article characterizes neuropsychologic functioning during remission in LLD.
The authors examined longitudinal performance on a comprehensive neuropsychologic battery in 56 nondemented subjects age 60 or older who initially presented with an episode of nonpsychotic unipolar major depression and 40 nondemented, age- and education-equated comparison subjects with no history of depression. Subjects were assessed at baseline (in a depressed state) and one year later (when remitted).
After one year, 45% of the LLD subjects were cognitively impaired despite remission of depression. Visuospatial ability, information-processing speed, and delayed memory were most frequently impaired; 94% of the patients who were impaired at baseline remained impaired one year later. Twenty-three percent of the patients who were cognitively normal while depressed developed impairment one year later.
Most older individuals who are cognitively impaired during a depressive episode remain impaired when their depression remits. In addition, a substantial proportion of older depressed individuals who are cognitively intact when depressed are likely to be impaired one year later, although their depression has remitted.
[Show abstract] [Hide abstract]
ABSTRACT: Since the renewed emphasis on the heterogeneity of geriatric depression and the impact on treatment response variability over a decade ago,1 neuroimaging methods have been increasingly applied to understand the underlying neurobiology of treatment response variability in geriatric depression.2 The application of neuroimaging methods has resulted in fundamental observations with respect to the neural circuitry and the role of the serotonin system. The observations that some patients remain symptomatic after adequate treatment with a selective serotonin uptake inhibitor (SSRI) ami that despite remission of mood symptoms, residual cognitive and other behavioral deficits persist, suggest that other neurochemical mechanisms may be involved. This review will focus on neurochemical imaging research in geriatric depression that has led to an initial understanding of the neurobiological mechanisms underlying remission of depression in late life. Future research directions to investigate the mechanisms underlying treatment resistance of mood and cognitive aspects of the illness will be discussed.Dialogues in clinical neuroscience 12/2008; 10(4).This article is viewable in ResearchGate's enriched formatRG Format enables you to read in context with side-by-side figures, citations, and feedback from experts in your field.
SourceAvailable from: PubMed Central[Show abstract] [Hide abstract]
ABSTRACT: Background Loneliness and depression are very common in the aged population. Both have negative impacts on cognition in the elderly. The present study aimed to investigate the effect of loneliness and depression on total as well as specific cognitive domains in cognitively normal male subjects. Material and Methods A total of 189 cognitively normal male subjects were recruited and underwent Cognitive Abilities Screening Instrument (CASI) and Wechsler Digit Span Task tests. Depression was assessed by the Geriatric Depression Scale-Short Form (GDS-SF) and loneliness by UCLA loneliness scales. Partial correlation test was used to explore the correlation between loneliness/depression and total as well as specific cognition function, with the controlled factors of age and education. Results Both depression and loneliness are negatively correlated with global cognitive function as evaluated with CASI (r=-0.227, p=0.002; r=-0.214, p=0.003, respectively). The domains of Attention, Orientation, Abstraction and judgment, and List-generating fluency of cognitive function were specifically associated with loneliness, and the domain of orientation was associated with depression after controlling the factors age and years of education. Conclusions Our findings suggest that loneliness and depression may have negative impacts on global and specific domains of cognitive function in non-demented elderly males. Both loneliness and depression should be actively recognized earlier and appropriately treated because they are significant sources of cognitive impairment in the elderly.Medical science monitor: international medical journal of experimental and clinical research 01/2015; 21:100-104. DOI:10.12659/MSM.891086 · 1.22 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: The first half of this paper briefly reviews the evidence that (i) stress precipitates depression by damaging the hippocampus, leading to changes in the activity of a distributed neural system involving, inter alia, the amygdala, the ventromedial and dorsolateral prefrontal cortex, the lateral habenula and ascending monoamine pathways, and (ii) antidepressants work by repairing the damaged hippocampus, thus restoring the normal balance of activity within that circuitry. In the second half of the paper we review the evidence that heightened vulnerability to depression, either because of a clinical history of depression or because of the presence of genetic, personality or developmental risk factors, also confers resistance to antidepressant drug treatment. Thus, although antidepressants provide an efficient means of reversing the neurotoxic effects of stress, they are much less effective in conditions where vulnerability to depression is elevated and the role of stress in precipitating depression is correspondingly lower. Consequently, the issue of vulnerability should feature much more prominently in antidepressant research. Most of the current animal models of depression are based on the induction of a depressive-like phenotype by stress, and pay scant attention to vulnerability. As antidepressants are relatively ineffective in vulnerable individuals, this in turn implies a need for the development of different clinical and preclinical methodologies, and a shift of focus away from the current preoccupation with the hippocampus as a target for antidepressant action in vulnerable patients.Behavioural Pharmacology 09/2014; 25(5 and 6):352-371. DOI:10.1097/FBP.0000000000000066 · 2.19 Impact Factor