Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients.
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ABSTRACT:
SUBMITTER: Brendel M
PROVIDER: S-EPMC5849231 | biostudies-literature | 2015 Apr
REPOSITORIES: biostudies-literature
Publications
Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients.
Brendel Matthias M Pogarell Oliver O Xiong Guoming G Delker Andreas A Bartenstein Peter P Rominger Axel A
European journal of nuclear medicine and molecular imaging 20150129 5
<h4>Purpose</h4>Late-life depression even in subsyndromal stages is strongly associated with Alzheimer's disease (AD). Furthermore, brain amyloidosis is an early biomarker in subjects who subsequently suffer from AD and can be sensitively detected by amyloid PET. Therefore, we aimed to compare amyloid load and glucose metabolism in subsyndromally depressed subjects with mild cognitive impairment (MCI).<h4>Methods</h4>[(18)F]AV45 PET, [(18)F]FDG PET and MRI were performed in 371 MCI subjects from ...[more]
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Project description:BackgroundCognitive impairment and depressive symptoms are highly prevalent after Intracerebral Hemorrhage (ICH). We leveraged Latent Profile Analysis (LPA) to identify profiles for cognitive decline and depression onset after ICH. We also investigated differences in clinical, genetic and neuroimaging characteristics across patients' profiles.MethodsWe analyzed data from the ICH study conducted at Massachusetts General Hospital between January 1998 and December 2019. We collected information from electronical health records, follow-up interviews, CT and MRI imaging, and APOE genotype. We conducted LPA and multinomial logistic regression analyses to: 1) identify distinct profiles for cognitive decline and depression onset after ICH; 2) identify clinical, neuroimaging and genetic factors predicting individuals' likelihood to express a specific profile.ResultsWe followed 784 ICH survivors for a median of 45.8 months. We identified four distinct profiles in cognitive and depressive symptoms after ICH: low depression and dementia risk, early-onset depression and dementia, late-onset depression and dementia, high depression with low dementia risk. Cerebral small vessel disease severity and APOE genotype were specifically associated with the late-onset profile (both p < 0.05). Acute hematoma characteristics (size, intraventricular extension) and functional disability were specifically associated with the early-onset profile (all p < 0.05).ConclusionWe identified four distinct profiles for cognitive and depressive symptoms after ICH, each displaying specific associations with individual patients' clinical, genetic and neuroimaging data. These associations reflect separate biological mechanisms influencing dementia and depression risk after ICH. Our findings support employing LPA in future ICH studies, and is likely applicable to stroke survivors at large.
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Project description:Previous research including meta-analytic efforts supports the assumption that depression is able to predict dementia. The mechanisms of this association still remain to be revealed. Some possible explanations as, for example, the glucocorticoid cascade hypothesis assumes that there are underlying changes at the cortical level that drive the association. Therefore, gradual levels of depressive symptoms may also predict gradual change (decline) in cognitive performance. However, testing both of these predictions (depressive symptoms lead to dementia, and depressive symptoms lead to cognitive decline, respectively) with the same data has to our knowledge not been done in the previous literature. A sample of 562 participants aged 65 or older was examined four times over a period of 3 years. Study participants completed established measures of depression and cognitive functioning. Results based on Cox regression analysis showed that depressive symptoms were not able to predict the conversion to dementia during the following 3 years. Additionally, structural equation models as well as latent change score models did not support the assumption that depressive symptoms predict cognitive decline, measured as a continuous variable. We discuss several possibilities to explain these findings including the potential and possible limits of the glucocorticoid cascade hypothesis.
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Project description:PurposeThe objective of this study was to determine how anxiety and/or depressive symptoms differentially affect specific cognitive domains over time in persons with subjective cognitive decline (SCD).DesignA longitudinal, observational study was conducted using data from the National Alzheimer's Coordinating Center-Uniform Data Set. Mean follow-up was 4.1 ± 2.4 years.MethodsUsing information from a total of 1401 participants (age 74.0 ± 8.2 years), linear mixed-effects regression models were used to assess longitudinal changes in global cognition, episodic memory, attention, language, and executive function by baseline psychological (anxiety [A] and/or depressive [D]) symptoms in individuals with SCD. Reference was the group having no symptoms (A-/D-).FindingsThe A+/D- group was not associated with any cognitive changes. The A-/D+ group was associated with a greater decline in episodic memory and executive function. The A+/D+ group had a greater decline in attention. Changes in global cognition and language were not predicted by any psychological symptoms.ConclusionsDepressive symptoms predicted lower episodic memory and executive function.Clinical relevanceNurses need to pay attention to depressive symptoms in older adults with SCD because managing depressive symptoms may help protect against cognitive decline more typical of early Alzheimer's dementia.
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Project description:ObjectiveTo determine whether the presence of depression predicts higher rate of progression to Alzheimer disease (AD) in patients with amnestic mild cognitive impairment (aMCI) and whether donepezil treatment beneficially affect this relationship.MethodsThe study sample was composed of 756 participants with aMCI from the 3-year, double-blind, placebo-controlled Alzheimer's Disease Cooperative Study drug trial of donepezil and vitamin E. Beck Depression Inventory (BDI) was used to assess depressive symptoms at baseline and participants were followed either to the end of study or to the primary endpoint of progression to probable or possible AD.ResultsCox proportional hazards regression, adjusted for age at baseline, gender, apolipoprotein genotype, and NYU paragraph delayed recall score, showed that higher BDI scores were associated with progression to AD (p = 0.03). The sample was stratified into depressed (BDI score > or =10; n = 208) and nondepressed (BDI <10; n = 548) groups. Kaplan-Meier analysis showed that among the depressed subjects, the proportion progressing to AD was lower for the donepezil group than the combined vitamin E and placebo groups at 1.7 years (p = 0.023), at 2.2 years (p = 0.025), and remained marginally lower at 2.7 years (p = 0.070). The survival curves among the three treatment groups did not differ within the nondepressed participants.ConclusionsResults suggest that depression is predictive of progression from amnestic mild cognitive impairment (aMCI) to Alzheimer disease (AD) and treatment with donepezil delayed progression to AD among depressed subjects with aMCI. Donepezil appears to modulate the increased risk of AD conferred by the presence of depressive symptoms.
| S-EPMC2697965 | biostudies-literature