scholarly journals Disability but not social support predicts cognitive deterioration in late-life depression

2014 ◽  
Vol 27 (5) ◽  
pp. 707-714 ◽  
Author(s):  
Meghan Riddle ◽  
Douglas R. McQuoid ◽  
Guy G. Potter ◽  
David C. Steffens ◽  
Warren D. Taylor

ABSTRACTBackground:Depression in late life is a risk factor for cognitive decline. Depression is also associated with increased disability and social support deficits; these may precede conversion to dementia and inform risk. In this study, we examined if baseline or one-year change in disability and social support predicted later cognitive deterioration.Methods:299 cognitively intact depressed older adults were followed for an average of approximately seven years. Participants received antidepressant treatment according to a standardized algorithm. Neuropsychological testing and assessment of disability and social support were assessed annually. Cognitive diagnosis was reviewed annually at a consensus conference to determine if participants remained cognitively normal, or if they progressed to either dementia or cognitively impaired, no dementia (CIND).Results:During study participation, 167 individuals remained cognitively normal (56%), 83 progressed to CIND (28%), and 49 progressed to dementia (16%). Greater baseline instrumental activities of daily living (IADL) deficits predicted subsequent conversion to a cognitive diagnosis (CIND or dementia). However, neither baseline measures nor one-year change in basic ADLs (BADLs) and social support predicted cognitive conversion. In post hoc analyses, two IADL measures (managing finances, preparing meals) significantly increased the odds of cognitive conversion.Conclusions:Greater IADL deficits predicted increased risk of cognitive conversion. Assessment of IADL deficits may provide clues about risk of later cognitive decline.

2015 ◽  
Vol 27 (5) ◽  
pp. 705-706
Author(s):  
Christina Bryant

It is well established that depression is common in late life and associated with a range of consequences for the individual and those close to them. These consequences include higher use of health services and declines in functional ability (Luppa et al., 2007), not to mention negative subjective experiences, such as reduced engagement with, and enjoyment of day-to-day activities. Depression in late life is a heterogeneous condition made more complex by the links between depression, cognitive decline and dementia. The “Vascular Depression Hypothesis” suggests that a subset of late life depressive disorders are caused by cerebrovascular disease (Taylor, 2014), but questions about the relationships between depression and cognitive decline remain unanswered. The paper chosen as the paper of the month in this issue of International Psychogeriatrics addresses one of these questions, namely, whether we can identify clinical signs and symptoms that predict cognitive decline in individuals diagnosed with depression. This question is of great clinical relevance, as not all patients and clinicians will have access to the neuroimaging or detailed neuropsychological assessment that could cast light on risk for cognitive deterioration.


2019 ◽  
Vol 31 (10) ◽  
pp. 1483-1489 ◽  
Author(s):  
Xiaomei Zhong ◽  
Zhangying Wu ◽  
Cong Ouyang ◽  
Wanyuan Liang ◽  
Ben Chen ◽  
...  

ABSTRACTObjectives:Cognitive impairment in late-life depression is common and associated with a higher risk of all-cause dementia. Late-life depression patients with comorbid cardiovascular diseases (CVDs) or related risk factors may experience higher risks of cognitive deterioration in the short term. We aim to investigate the effect of CVDs and their related risk factors on the cognitive function of patients with late-life depression.Methods:A total of 148 participants were recruited (67 individuals with late-life depression and 81 normal controls). The presence of hypertension, coronary heart disease, diabetes mellitus, or hyperlipidemia was defined as the presence of comorbid CVDs or related risk factors. Global cognitive functions were assessed at baseline and after a one-year follow-up by the Mini-Mental State Examination (MMSE). Global cognitive deterioration was defined by the reliable change index (RCI) of the MMSE.Results:Late-life depression patients with CVDs or related risk factors were associated with 6.8 times higher risk of global cognitive deterioration than those without any of these comorbidities at a one-year follow-up. This result remained robust after adjusting for age, gender, and changes in the Hamilton Depression Rating Scale (HAMD) scores.Conclusions:This study suggests that late-life depression patients with comorbid CVDs or their related risk factors showed a higher risk of cognitive deterioration in the short-term (one-year follow up). Given that CVDs and their related risk factors are currently modifiable, active treatment of these comorbidities may delay rapid cognitive deterioration in patients with late-life depression.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
M. Ly ◽  
H. T. Karim ◽  
J. T. Becker ◽  
O. L. Lopez ◽  
S. J. Anderson ◽  
...  

AbstractLate-life depression (LLD) is associated with an increased risk of developing dementia; however, it is not known whether individuals with a history of LLD exhibit a more rapid rate of cognitive decline. We aimed to determine whether those with LLD experienced faster cognitive decline compared with never-depressed control (NDC) participants from the community and whether stratification of LLD into early-onset depression (EOD) and late-onset depression (LOD) subtypes revealed differing rates and domain-specific expression of cognitive decline. We conducted a prospective, longitudinal study where 185 participants with LLD (remitted) and 114 NDC were followed for 5 years on average. EOD was defined as having first lifetime depressive episode at <60years and LOD at ≥60years. Every year, participants underwent comprehensive neuropsychological assessment. Composite scores for each cognitive domain were calculated through averaging standardized scores across tests. LLD compared to NDC demonstrated significant baseline impairment but did not decline more rapidly. EOD were significantly impaired in attention/processing speed and global cognitive function at baseline but did not experience more rapid decline as compared to NDC. Those with LOD compared to both NDC and EOD performed worse in all domains at baseline and experienced more rapid decline in verbal skills and delayed memory ability. Our findings suggest that baseline impairment may lower the threshold for those with LLD to develop dementia. EOD and LOD may represent distinct phenotypes of cognitive impairment with differing neural substrates. LOD may represent a distinct phenotype with a more rapid decline in verbal skills and delayed memory.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gwenn S. Smith ◽  
Clifford I. Workman ◽  
Hillary Protas ◽  
Yi Su ◽  
Alena Savonenko ◽  
...  

AbstractDepression in late-life is associated with increased risk of cognitive decline and development of all-cause dementia. The neurobiology of late-life depression (LLD) may involve both neurochemical and neurodegenerative mechanisms that are common to depression and dementia. Transgenic amyloid mouse models show evidence of early degeneration of monoamine systems. Informed by these preclinical data, the hypotheses were tested that a spatial covariance pattern of higher beta-amyloid (Aβ) and lower serotonin transporter availability (5-HTT) in frontal, temporal, and parietal cortical regions would distinguish LLD patients from healthy controls and the expression of this pattern would be associated with greater depressive symptoms. Twenty un-medicated LLD patients who met DSM-V criteria for major depression and 20 healthy controls underwent PET imaging with radiotracers for Aβ ([11C]-PiB) and 5-HTT ([11C]-DASB). A voxel-based multi-modal partial least squares (mmPLS) algorithm was applied to the parametric PET images to determine the spatial covariance pattern between the two radiotracers. A spatial covariance pattern was identified, including higher Aβ in temporal, parietal and occipital cortices associated with lower 5-HTT in putamen, thalamus, amygdala, hippocampus and raphe nuclei (dorsal, medial and pontine), which distinguished LLD patients from controls. Greater expression of this pattern, reflected in summary 5-HTT/Aβ mmPLS subject scores, was associated with higher levels of depressive symptoms. The mmPLS method is a powerful approach to evaluate the synaptic changes associated with AD pathology. This spatial covariance pattern should be evaluated further to determine whether it represents a biological marker of antidepressant treatment response and/or cognitive decline in LLD patients.


2021 ◽  
Vol 29 (1) ◽  
pp. 66-77 ◽  
Author(s):  
Kevin J. Manning ◽  
Grace Chan ◽  
David C. Steffens ◽  
Cortnee W. Pierce ◽  
Guy G. Potter

2014 ◽  
Vol 26 (9) ◽  
pp. 1501-1509 ◽  
Author(s):  
Celia F. Hybels ◽  
Carl F. Pieper ◽  
Lawrence R. Landerman ◽  
Martha E. Payne ◽  
David C. Steffens

ABSTRACTBackground:The association between disability and depression is complex, with disability well established as a correlate and consequence of late life depression. Studies in community samples report that greater volumes of cerebral white matter hyperintensities (WMHs) seen on brain imaging are linked with functional impairment. These vascular changes are also associated with late life depression, but it is not known if depression is a modifier in the relationship between cerebrovascular changes and functional impairment.Methods:The study sample was 237 older adults diagnosed with major depression and 140 never depressed comparison adults, with both groups assessed at study enrollment. The dependent variable was the number of limitations in basic activities of daily living (ADL), instrumental ADLs, and mobility tasks. The independent variable was the total volume of cerebral white matter lesions or hyperintensities assessed though magnetic resonance imaging.Results:In analyses controlling for age, sex, race, high blood pressure, and cognitive status, a greater volume of WMH was positively associated with the total number of functional limitations as well as the number of mobility limitations among those older adults with late life depression but not among those never depressed, suggesting the association between WMH volume and functional status differs in the presence of late life depression.Conclusions:These findings suggest older patients with both depression and vascular risk factors may be at an increased risk for functional decline, and may benefit from management of both cerebrovascular risk factors and depression.


2016 ◽  
Vol 47 (4) ◽  
pp. 690-702 ◽  
Author(s):  
A. Brailean ◽  
M. J. Aartsen ◽  
G. Muniz-Terrera ◽  
M. Prince ◽  
A. M. Prina ◽  
...  

BackgroundCognitive impairment and depression often co-occur in older adults, but it is not clear whether depression is a risk factor for cognitive decline, a psychological reaction to cognitive decline, or whether changes in depressive symptoms correlate with changes in cognitive performance over time. The co-morbid manifestation of depression and cognitive impairment may reflect either a causal effect or a common cause, depending on the specific symptoms experienced and the cognitive functions affected.MethodThe study sample comprised 1506 community-dwelling older adults aged ⩾65 years from the Longitudinal Aging Study Amsterdam (LASA). We conducted cross-domain latent growth curve analyses to examine longitudinal associations between late-life depression dimensions (i.e. depressed affect, positive affect, and somatic symptoms) and specific domains of cognitive functioning (i.e. processing speed, inductive reasoning, immediate recall, and delayed recall).ResultsPoorer delayed recall performance at baseline predicted a steeper increase in depressed affect over time. Steeper decline in processing speed correlated with a steeper increase in somatic symptoms of depression over time.ConclusionsOur findings suggest a prospective association between memory function and depressed affect, whereby older adults may experience an increase in depressed affect in reaction to poor memory function. Somatic symptoms of depression increased concurrently with declining processing speed, which may reflect common neurodegenerative processes. Our findings do not support the hypothesis that depression symptoms may be a risk factor for cognitive decline in the general population. These findings have potential implications for the treatment of late-life depression and for the prognosis of cognitive outcomes.


Author(s):  
Claudio Liguori ◽  
Mariangela Pierantozzi ◽  
Agostino Chiaravalloti ◽  
Giulia M. Sancesario ◽  
Nicola B. Mercuri ◽  
...  

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