(1) Background: There is a need for a brief assessment of cognitive function, both in patient care and scientific research, for which the Montreal Cognitive Assessment (MoCA) is a psychometrically reliable and valid tool. However, fine-grained normative data allowing for adjustment for age, education, and/or sex are lacking, especially for its Memory Index Score (MIS). (2) Methods: A total of 820 healthy individuals aged 18–91 (366 men) completed the Dutch MoCA (version 7.1), of whom 182 also completed the cued recall and recognition memory subtests enabling calculation of the MIS. Regression-based normative data were computed for the MoCA Total Score and MIS, following the data-handling procedure of the Advanced Neuropsychological Diagnostics Infrastructure (ANDI). (3) Results: Age, education level, and sex were significant predictors of the MoCA Total Score (Conditional R2 = 0.4, Marginal R2 = 0.12, restricted maximum likelihood (REML) criterion at convergence: 3470.1) and MIS (Marginal R2 = 0.14, REML criterion at convergence: 682.8). Percentile distributions are presented that allow for age, education and sex adjustment for the MoCA Total Score and the MIS. (4) Conclusions: We present normative data covering the full adult life span that can be used for the screening for overall cognitive deficits and memory impairment, not only in older people with or people at risk of neurodegenerative disease, but also in younger individuals with acquired brain injury, neurological disease, or non-neurological medical conditions.
Cognitive reserve (CR) is known to reduce or even protect against the negative effects of aging on cognitive functioning. Nonetheless, little is known about how CR influences the relationship between different cognitive abilities and age in the old–old. The goal of the present study was, therefore, to test the hypothesis whether, in the old–old, CR still modifies the relationship between age and cognitive functioning. Eighty-three adults (aged 71–94) without mild cognitive impairment or dementia residing in residential care facilities completed a detailed neuropsychological test battery. CR was estimated using a combination of educational attainment and an estimation of verbal intelligence. Moderation analyses revealed a significant effect for fluency and a trend for flexibility, showing that the negative relationship between age and cognitive performance is reduced as the level of CR increases. These results demonstrate that CR still influences the relationship between age and executive functions in adults of advanced age.
Background: Variability in cognitive functions in healthy and pathological aging is often explained by educational attainment. However, it remains unclear to which extent different disease states alter protective effects of education. We aimed to investigate whether protective effects of education on cognition depend on (1) clinical diagnosis severity, and (2) the neuropathological burden within a diagnosis in a memory clinic setting.Methods: In this cross-sectional study, we included 108 patients with subjective cognitive decline [SCD, median age 71, IQR (66–78), 43% men], 190 with mild cognitive impairment [MCI, median age 78, IQR (73–82), 44% men], and 245 with Alzheimer’s disease dementia (AD) [median age 80, IQR (76–84), 35% men]. We combined visual ratings of hippocampal atrophy, global atrophy, and white matter hyperintensities on MRI into a single neuropathology score. To investigate whether the contribution of education to cognitive performance differed across SCD, MCI, and AD, we employed several multiple linear regression models, stratified by diagnosis and adjusted for age, sex, and neurodegeneration. We re-ran each model with an additional interaction term to investigate whether these effects were influenced by neuropathological burden for each diagnostic group separately. False discovery rate (FDR) corrections for multiple comparisons were applied.Results: We observed significant positive associations between education and performance for global cognition and executive functions (all adjusted p-values < 0.05). As diagnosis became more severe, however, the strength of these associations decreased (all adjusted p-values < 0.05). Education related to episodic memory only at relatively lower levels of neuropathology in SCD (β = −0.23, uncorrected p = 0.02), whereas education related to episodic memory in those with higher levels of neuropathology in MCI (β = 0.15, uncorrected p = 0.04). However, these interaction effects did not survive FDR-corrections.Conclusions: Altogether, our results demonstrated that positive effects of education on cognitive functioning reduce with diagnosis severity, but the role of neuropathological burden within a particular diagnosis was small and warrants further investigation. Future studies may further unravel the extent to which different dimensions of an individual’s disease severity contribute to the waxing and waning of protective effects in cognitive aging.
We characterize the associations of total cerebral small vessel disease (SVD) burden with brain structure, trajectories of vascular risk factors, and cognitive functions in mid-to-late life. Participants were 623 community-dwelling adults from the Whitehall II Imaging Sub-study with multi-modal MRI (mean age 69.96, SD = 5.18, 79% men). We used linear mixed-effects models to investigate associations of SVD burden with up to 25-year retrospective trajectories of vascular risk and cognitive performance. General linear modelling was used to investigate concurrent associations with grey matter (GM) density and white matter (WM) microstructure, and whether these associations were modified by cognitive status (Montreal Cognitive Asessment [MoCA] scores of < 26 vs. ≥ 26). Severe SVD burden in older age was associated with higher mean arterial pressure throughout midlife (β = 3.36, 95% CI [0.42-6.30]), and faster cognitive decline in letter fluency (β = −0.07, 95% CI [−0.13–−0.01]), and verbal reasoning (β = −0.05, 95% CI [−0.11–−0.001]). Moreover, SVD burden was related to lower GM volumes in 9.7% of total GM, and widespread WM microstructural decline (FWE-corrected p < 0.05). The latter association was most pronounced in individuals who demonstrated cognitive impairments on MoCA (MoCA < 26; F3,608 = 2.14, p = 0.007). These findings highlight the importance of managing midlife vascular health to preserve brain structure and cognitive function in old age.
Introduction It is unclear why cerebral small vessel disease (SVD) leads to lacunar stroke in some and to non–lobar intracerebral hemorrhage (ICH) in others. We investigated differences in MRI markers of SVD in patients with lacunar stroke or non–lobar ICH. Patients and methods We included patients from two prospective cohort studies with either lacunar stroke (RUN DMC) or non–lobar ICH (FETCH). Differences in SVD markers (white matter hyperintensities [WMH], lacunes, cerebral microbleeds [CMB]) between groups were investigated with univariable tests; multivariable logistic regression analysis, adjusted for age, sex, and vascular risk factors; spatial correlation analysis and voxel–wise lesion symptom mapping. Results We included 82 patients with lacunar stroke (median age 63, IQR 57–72) and 54 with non-lobar ICH (66, 59–75). WMH volumes and distribution were not different between groups. Lacunes were more frequent in patients with a lacunar stroke (44% vs. 17%, adjusted odds ratio [aOR] 5.69, 95% CI [1.66–22.75]) compared to patients with a non–lobar ICH. CMB were more frequent in patients with a non–lobar ICH (71% vs. 23%, aOR for lacunar stroke vs non–lobar ICH 0.08 95% CI [0.02–0.26]), and more often located in non–lobar regions compared to CMB in lacunar stroke. Discussion Although we obserd different types of MRI markers of SVD within the same patient, ischemic markers of SVD were more frequent in the ischemic type of lacunar stroke, and hemorrhagic markers were more prevalent in the hemorrhagic phenotype of non-lobar ICH. Conclusion There are differences between MRI markers of SVD between patients with a lacunar stroke and those with a non-lobar ICH.
Background: Globally, up to 40% of dementia cases may be prevented if several key risk factors, such as low education and obesity, are targeted. This has motivated interest into the development of risk scores that aim to quantify an individual's risk of developing dementia within a given time frame. However, translation to a clinical setting has been hampered by either a lack of external validation, poor out-of-sample performance, or the integration of measures (e.g., MRI, cognitive testing) that are costly or time intensive to administer.This study aimed to develop a novel dementia risk score suitable for a primary care setting and compare its discrimination accuracy with other risk scores. Method: 208,108 UK Biobank (UKB) participants were examined, with cases of incident dementia (mean time to diagnosis ± SD = 5.91 years ± 2.02) identified through self-report, hospital inpatient records and death certificates (n = 1,270, 0.6%). The dataset was randomly split into a training (80%) and test set (20%). Potential predictors (n = 30) included Apolipoprotein E4 (APOE4) status and cardiovascular, medical and lifestyle factors collected at baseline. Logistic LASSO regression was employed for variable selection and logistic regression was then used to derive beta coefficients for each predictor included in the UKB dementia risk score (UKB-DRS). The area under the curve (i.e., AUC) was used to compare the discriminative ability of the UKB-DRS to the CAIDE, ANU-ADRI, Dementia Risk Score (i.e., DRS) and Framingham risk score, in both the test set and the Whitehall II study (WHIII, n = 2,974), which served as an external dataset. Result: The UKB-DRS consisted of age, sex, education, APOE4 status, a medical history of diabetes, stroke and depression and a family history of dementia. The UKB-DRS demonstrated good discrimination accuracy in both the test set (AUC [95% ] = 0.79 [0.77, 0.82]) and external dataset (AUC [95% CI] = 0.83 [0.79,0.87]). Additionally, the UKB-DRS outperformed all other risk scores (the DRS had the next best AUC [95% CI]: UKB = 0.77 [0.74, 0.8]; WHII = 0.77 [0.73, 0.81]). Conclusion:This study contributes a novel dementia risk score that may be used to guide primary prevention strategies.
Remembering to perform a delayed intention is termed prospective memory (PM). Often delayed intentions are shared by more than one person; however, there is a dearth of studies examining PM in social settings. We aimed to investigate whether the potential consequences of one's behavior across diverse group settings influence PM performance in event-and time-based tasks. A total of 207 participants were randomly allocated to either an individual, collaborative, or collaborative plus penalty motivation condition and were tested in a 2-or 3-person setting. For the time-based PM task, participants responded less timely in the individual motivation condition, whereas there was no difference between the collaborative motivation conditions. No significant effects were found for motivation condition on the event-based task or for group size on PM performance. Analyses of ongoing task performance revealed that participants' attention allocation policies change depending on how individuals prioritize the ongoing and PM tasks.
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