Depressive symptoms as predictor of dementia versus continuous cognitive decline: a 3-year prospective study.
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ABSTRACT:
SUBMITTER: Neubauer AB
PROVIDER: S-EPMC5549226 | biostudies-other | 2013 Mar
REPOSITORIES: biostudies-other
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Project description:We report the cognitive decline in persons diagnosed with mild dementia with Lewy bodies (DLB) and mild Alzheimer's disease (AD) during 5 years of annual follow-ups.Patients were recruited into the study from geriatric, psychiatric and neurology clinics in Western Norway during 2005-2013. They were diagnosed according to clinical consensus criteria, based on standardised clinical rating scales. Autopsy-based diagnoses were available for 20 cases. Cognitive decline for up to 5 years was assessed using the Clinical Dementia Rating (CDR) scale and the Mini-Mental State Examination (MMSE). Survival analysis including Cox regression (time to reach severe dementia) and linear mixed-effects (lme) modelling were used to model the decline on MMSE.At least one follow-up assessment was available for 67 patients with DLB and 107 patients with AD, with a median follow-up time of 4.3 years. The time to reach severe dementia was significantly shorter in DLB (median 1793 days) compared with AD (1947 days; p=0.033), and the difference remained significant in the multiple Cox regression analysis (HR=2.0, p<0.02). In the adjusted lme model, MMSE decline was faster in DLB (annual decline 4.4 points) compared with AD (3.2 points; p<0.008).Our findings show that from the mild dementia stage, patients with DLB have a more rapid cognitive decline than in AD. Such prognostic information is vital for patients and families and crucial for planning clinical trials and enabling health economic modelling.
| S-EPMC4780061 | biostudies-other
Project description:PurposeLate-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).Methods[(18)F]AV45 PET, [(18)F]FDG PET and MRI were performed in 371 MCI subjects from the Alzheimer's Disease Neuroimaging Initiative Subjects were judged β-amyloid-positive (Aβ+; 206 patients) or β-amyloid-negative (Aβ-; 165 patients) according to [(18)F]AV45 PET. Depressive symptoms were assessed by the Neuropsychiatric Inventory Questionnaire depression item 4. Subjects with depressive symptoms (65 Aβ+, 41 Aβ-) were compared with their nondepressed counterparts. Conversion rates to AD were analysed (mean follow-up time 21.5 ± 9.1 months) with regard to coexisting depressive symptoms and brain amyloid load.ResultsAβ+ depressed subjects showed large clusters with a higher amyloid load in the frontotemporal and insular cortices (p < 0.001) with coincident hypermetabolism (p < 0.001) in the frontal cortices than nondepressed subjects. Faster progression to AD was observed in subjects with depressive symptoms (p < 0.005) and in Aβ+ subjects (p < 0.001). Coincident depressive symptoms additionally shortened the conversion time in all Aβ+ subjects (p < 0.005) and to a greater extent in those with a high amyloid load (p < 0.001).ConclusionOur results clearly indicate that Aβ+ MCI subjects with depressive symptoms have an elevated amyloid load together with relative hypermetabolism of connected brain areas compared with cognitively matched nondepressed individuals. MCI subjects with high amyloid load and coexistent depressive symptoms are at high risk of faster conversion to AD.
| S-EPMC5849231 | biostudies-literature
Project description:The aim was to investigate the pattern and rate of cognitive decline across distinctive trajectories of depressive symptoms in older adults. In this prospective multinational cohort study on 69,066 participants (on average 64 years at baseline, 55% women), assessments of cognitive functions (immediate recall, delayed recall, verbal fluency) and depressive symptoms (EURO-D scale) were conducted at 2-year intervals. The trajectories of depressive symptoms were obtained using latent growth mixture modelling, cognitive decline was assessed using smoothing splines and linear mixed effects models. Four distinct trajectories of depressive symptoms were identified: constantly low (n = 49,660), constantly high (n = 2999), increasing (n = 6828) and decreasing (n = 9579). Individuals with increasing and constantly high depressive symptoms showed linear cognitive decline, while those with constantly low and decreasing depressive symptoms had fluctuating cognition. Participants with increasing depressive symptoms had the fastest decline, while those with decreasing symptoms were spared from decline in cognition. This study suggests that the pattern as well as the rate of cognitive decline co-occurs with specific patterns of changes in depressive symptoms over time. The most pronounced cognitive decline is present in individuals, in whom depressive symptoms increase late in life. Unique mechanisms of cognitive decline may exist for subgroups of the population, and are associated with the trajectory of depressive symptoms.
| S-EPMC7705007 | biostudies-literature
Project description:ObjectivesLate-life depression is a comorbidity that may co-occur in older adults with hearing loss-each has prevalent and independent modifiable risk factors for dementia.MethodsUsing data from 1,820 Health, Aging and Body Composition study participants (74 ± 2.8 years, 38% Black race), we compared the hearing loss-dementia/cognitive decline relationship between those with normal hearing/mild hearing loss and those with moderate or greater hearing loss. Using linear mixed-effects and Cox proportional hazard models, we investigated if the associations between hearing loss and cognitive decline or dementia (Modified Mini-Mental State [3MS] Examination and Digit Symbol Substitution Test [DSST]) differed by the presence or absence of depressive symptoms. Depressive symptoms were defined as Center for Epidemiologic Study-Depression scale 10 ≥10 at one or more visits from Years 1-5. Algorithmic incident dementia was defined using medication use, hospitalizations, and cognitive test scores. Audiometric hearing loss was measured at Year 5 and categorized as normal/mild versus moderate or greater hearing loss.ResultsHaving both hearing loss and depressive symptoms (vs. having neither) was associated with faster rates of decline in 3MS Examination (β = -0.30; 95% confidence interval [CI]: -0.78, -0.19) and DSST (β = -0.35; 95% CI: -0.67, -0.03) over 10 years of follow-up. Having both hearing loss and depressive symptoms (vs. neither) was associated with increased risk (hazard ratio [HR]: 2.91; 95% CI: 1.59, 5.33 vs. HR: 1.54; 95% CI: 1.10, 2.15 hearing loss only and HR: 2.35; 95% CI: 1.56, 3.53 depressive symptoms only) of incident dementia in multivariable-adjusted Cox proportional hazards models.DiscussionComorbid conditions among hearing-impaired older adults should be considered and may aid in dementia prevention and management strategies.
| S-EPMC9071460 | biostudies-literature
Project description:BackgroundDepressive symptoms and mild cognitive impairment (MCI) are highly prevalent in rural China. The study aimed to investigate the longitudinal associations between changes in depressive symptoms and cognitive decline and MCI incidence among Chinese rural elderly individuals.MethodsA 2-year follow-up study was conducted among 1,477 participants from the Anhui Healthy Longevity Survey (AHLS). Depressive symptoms were assessed by the 9-item Patient Health Questionnaire (PHQ-9), and cognitive status was evaluated by the Mini Mental State Examination (MMSE). Multivariable linear regression and logistic regression were employed.ResultsEvery 1-unit PHQ-9 score increase was significantly associated with more cognitive decline (β = 0.157, 95% CI: 0.092, 0.221, p < 0.001) and a higher risk of MCI incidence (OR = 1.063, 95% CI: 1.025, 1.103, p = 0.001). The participants who experienced worsening of depression symptoms had a larger decline in the 2-year MMSE score (β = 0.650, 95% CI: 0.039, 1.261, p = 0.037) and elevated risks of incident MCI (OR = 1.573, 95% CI: 1.113, 2.223, p = 0.010).LimitationsScreening tools rather than standard diagnostic procedures were used in the study. Moreover, the long-term associations still need further exploration since the follow-up time was short.ConclusionsIncreased depressive symptoms were associated with more cognitive decline and higher risks of incident MCI among Chinese rural residents.
| S-EPMC9326072 | biostudies-literature
Project description:BACKGROUND:Subjective cognitive decline (SCD) and anxiety symptoms both predict neurocognitive disorders, but the two correlate strongly with each other. It is unclear whether they reflect two independent disease processes in the development of neurocognitive disorders and hence deserve separate attention. This cohort study examined whether SCD and anxiety symptoms demonstrate independent risks of mild cognitive disorder and dementia (MCI/dementia). METHODS:The study included 14,066 participants aged ??50?years and diagnosed with normal cognition at baseline, recruited from Alzheimer's Disease Centers across the USA. The participants were evaluated for SCD and anxiety symptoms at baseline and followed up almost annually for incident MCI/dementia (median follow-up 4.5?years; interquartile range 2.2-7.7?years). SCD and anxiety symptoms were included in Cox regression to investigate their independent risks of MCI/dementia. RESULTS:SCD and anxiety symptoms demonstrated independent risks of MCI/dementia, with HR 1.9 (95% CI 1.7-2.1) and 1.3 (95% CI 1.2-1.5), respectively. Co-occurring SCD and anxiety symptoms demonstrated the highest risk (HR 2.4, 95% CI 1.9-2.9)-participants in this group had a 25% probability of developing MCI/dementia by 3.1?years (95% 2.4-3.7), compared to 8.2?years among those without SCD or anxiety (95% CI 7.9-8.6). The results remained robust even in the sensitivity analyses that took into account symptom severity and consistency of symptoms in the first 2 annual visits. CONCLUSIONS:The findings suggest that clinicians should not dismiss one over the other when patients present with both SCD and anxiety and that both constructs may potentially be useful to identify high-risk populations for preventive interventions and trials. The findings also point to the need for further research to clarify on the neurobiological distinctions between SCD and anxiety symptoms, which may potentially enrich our understanding on the pathogenesis of neurocognitive disorders.
| S-EPMC7488541 | biostudies-literature
Project description:To clarify the relationship between depressive symptoms and the clinical and neuropathologic manifestations of dementia.In a clinical-pathologic cohort study, 1,764 older persons without cognitive impairment at enrollment completed annual clinical evaluations for a mean of 7.8 years. The evaluations included assessment of depressive symptoms (10-item Center for Epidemiological Studies Depression Scale) and cognitive function (battery of 17 performance tests). A total of 582 individuals died during follow-up and underwent a uniform neuropathologic examination to quantify ?-amyloid plaques and tau tangle density in multiple brain regions and identify neocortical Lewy bodies, hippocampal sclerosis, and gross and microscopic cerebral infarcts.Level of depressive symptoms slightly increased during follow-up. Incident mild cognitive impairment (52.2%) was associated with higher level of depressive symptoms before the diagnosis but not with change in symptoms after the diagnosis; incident dementia (17.9%) was associated with higher symptom level before dementia onset and with more rapid decline in symptoms after dementia onset. None of the neuropathologic markers was related to level of depressive symptoms or change in symptoms over time. In a mixed-effects model adjusted for the neuropathologic markers, higher level of depressive symptoms averaged over evaluations was associated with more rapid global cognitive decline, accounting for 4.4% of the variability in decline not attributable to the neuropathologic markers. Depressive symptoms did not modify the association of the neuropathologic markers with cognitive decline.In old age, depressive symptoms have an association with cognitive decline that is independent of the neuropathologic hallmarks of dementia.
| S-EPMC4150132 | biostudies-literature
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.
| S-EPMC8662844 | biostudies-literature
Project description:BackgroundDepressive symptoms may increase risk for dementia, but findings are controversial because late-life depression may be a prodromal dementia symptom. Life course data on depression and dementia risk may clarify this association; however, data is limited.ObjectiveTo impute adult depressive symptoms trajectories across adult life stages and estimate the association with cognitive impairment and decline.MethodsUsing a pooled study of 4 prospective cohorts (ages 20-89), we imputed adult life course depressive symptoms trajectories based on Center for Epidemiologic Studies Depression Scale-10 (CESD-10) and calculated time-weighted averages for early adulthood (ages 20-49), mid-life (ages 50-69), and late-life (ages 70-89) for 6,122 older participants. Adjusted pooled logistic and mixed-effects models estimated associations of imputed depressive symptoms with two cognitive outcomes: cognitive impairment defined by established criteria and a composite cognitive score.ResultsIn separate models, elevated depressive symptoms in each life stage were associated with cognitive outcomes: early adulthood OR for cognitive impairment = 1.59 (95%CI: 1.35,1.87); mid-life OR = 1.94 (95%CI:1.16, 3.26); and late-life OR = 1.77 (95%CI:1.42, 2.21). When adjusted for depressive symptoms in the other life-stages, elevated depressive symptoms in early adulthood (OR = 1.73; 95%CI: 1.42,2.11) and late-life (OR = 1.43; 95%CI: 1.08,1.89) remained associated with cognitive impairment and were also associated with faster rates of cognitive decline (p < 0.05).ConclusionImputing depressive symptom trajectories from pooled cohorts may help expand data across the life course. Our findings suggest early adulthood depressive symptoms may be a risk factor for cognitive impairment independent of mid- or late-life depressive symptoms.
| S-EPMC9095065 | biostudies-literature
Project description:BACKGROUND: Apolipoprotein E (APOE) polymorphisms are unequivocally associated with risk for Alzheimer's disease (AD). It is crucial to understand how this genetic factor affects dementia risk in the general population, as well as in narrowly diagnosed, selected, patient groups. METHODS: We assessed the cross sectional association between APOE genotype and dementia status in a community based sample, the MRC Cognitive Function and Ageing Study (MRC CFAS). In addition, we tested the effects of APOE genotypes on the differences in MMSE scores between the first and third assessment waves (about six years apart), an index of cognitive decline. RESULTS: The APOE epsilon4 allele conferred increased risk for dementia (OR=1.5, 95% CI=1.1 to 2.2) compared to epsilon3 in the MRC CFAS sample. Compared with APOE epsilon3/epsilon 3 subjects, those with the epsilon3/epsilon4 genotypes were not at significantly higher risk for dementia (OR=1.1, 95% CI=0.6 to 1.9), although epsilon4/epsilon4 subjects were (OR= 3.8, 95% CI=1.0 to 14.0). Risk estimates were not different between men and women. Notably, our risk estimates for dementia were significantly lower than those reported for a diagnosis of Alzheimer's disease. MMSE scores at wave 3 and the difference in MMSE between baseline and at the third assessment wave were not different across APOE genotypes. INTERPRETATION: The APOE epsilon4 allele is a weaker predictor for dementia in the general population than for AD. This may be because dementia can be caused by non-AD pathological processes and because most prevalent dementia occurs at an age when the APOE epsilon4 effect on AD risk (and therefore dementia) has started to decline.
| S-EPMC1735244 | biostudies-other