Decline across different domains of cognitive function in normal ageing: Results of a longitudinal population-based study using CAMCOG

ABSTRACT Dementia is an important cause of disability in the elderly[ There is evidence that cognitive impairment in dementia is on a continuum with cognitive impairment in the non!demented elderly[ In order to investigate this possibility\ we need detailed knowledge about the population distribution of cognitive function and change in cognitive function[ The aim of this study is to describe the change in di}erent domains of cognitive function over 3 years in a population! based sample of non!demented elderly people\ and to investigate the e}ect of sociodemographic variables and baseline cognitive function on change in each of the cognitive domains[ Respondents from two group general practice lists "n 492# were interviewed using the Cambridge Cognitive Examination "CAMCOG# at the incidence wave of the Cambridge City Over!64 Cohort Study and after a mean time period of 2[8 years[ One hundred and thirty _ve of 101 non!demented subjects seen at follow!up completed the CAMCOG at both interviews[ The annual rate of change in total CAMCOG score was −0[5 points per year "p ³ 9[990#[ There was statistically signi_cant decline in all of the CAMCOG subscales[ Greater decline in the Memory subscale was associated with less education "p 9[92#[ Greater decline in the Attention:Calculation subscale was associated with manual social class "p 9[94#[ Greater decline in the Perception subscale was associated with older age "p 9[92#[ Decline in speci_c cognitive domains may indicate a reversible phase of cognitive impairment and deserves further investigation

Cohort differences in disease and disability in the young-old: findings from the MRC Cognitive Function and Ageing Study (MRC-CFAS).

BACKGROUND: Projections of health and social care need are highly sensitive to assumptions about cohort trends in health and disability. We use a repeated population-based cross-sectional study from the Cambridgeshire centre of the UK Medical Research Council Cognitive Function and Ageing Study to investigate trends in the health of the young-old UK population METHODS: Non-overlapping cohorts of men and women aged 65-69 years in 1991/2 (n = 689) and 1996/7 (n = 687) were compared on: self-reported diseases and conditions; self-rated health; mobility limitation; disability by logistic regression and four-year survival by Cox Proportional Hazards Regression models, with adjustments for differences in socio-economic and lifestyle factors. RESULTS: Survival was similar between cohorts (HR: 0.91, 95% CI: 0.62 to 1.32). There was a significant increase in the number of conditions reported between cohorts, with more participants reporting 3 or more conditions in the new cohort (14.2% vs. 10.1%). When individual conditions were considered, there was a 10% increase in the reporting of arthritis and a significant increase in the reporting of chronic airways obstruction (OR: 1.36, 95% CI: 1.04 to 1.78). CONCLUSION: This study provides evidence of rising levels of ill-health, as measured by the prevalence of self-reported chronic conditions, in the newer cohorts of the young-old. Though changes in diagnosis or reporting of disease cannot, as yet, be excluded, to better understand whether our findings reflect real increases in ill-health, investment should be made into improved population-based databases, linking self-report and objective measures of health and function, and including those in long-term care

Lewy Body Variant of Alzheimer's Disease: Selective Neocortical Loss of t-SNARE Proteins and Loss of MAP2 and α-Synuclein in Medial Temporal Lobe

Lewy bodies (LBs) appear in the brains of nondemented individuals and also occur in a range of neurodegenerative disorders, such as dementia with Lewy bodies (DLB) and Parkinson's disease. A number of people with a definite diagnosis of Alzheimer's disease (AD) also exhibit these intraneuronal inclusions in allo- and/or neocortical areas. The latter, referred to as Lewy body variant of AD (LBV), bears a clinical resemblance to AD in terms of age at onset, duration of illness, cognitive impairment, and illness severity. Since the presence of LBs is accompanied by neuronal cytoskeleton changes, it is possible that the latter may influence neuronal connectivity via alterations to the synaptic network. To address this, we examined the expression of synaptic proteins (synaptophysin, syntaxin, SNAP-25, and α-synuclein) and two cytoskeletal proteins (tau and MAP2) in the brain tissue of subjects enrolled in a population-based autopsy study (n = 47). They were divided into groups with no memory problems (control group, n = 15), LBV (n = 5), AD devoid of LBs (n = 17), cerebrovascular dementia (n = 3), and mixed dementia (n = 7). The LBV and AD groups had a similar degree of cognitive impairment and neuropathological staging in terms of Braak staging and CERAD score. In comparison with the control group and the dementia groups without LBs, the LBV group had significantly lower levels of syntaxin and SNAP-25 (23%) in the neocortex, and depletion of MAP2 (64%), SNAP-25 (34%), and α-synuclein (44%) proteins in the medial temporal lobes. These findings suggest that the t-SNARE complex deficit present in LBV may be associated with the presence of LB-related pathology and may explain the more profound cholinergic loss seen in these patients

Cohort differences in disease and disability in the young-old: findings from the MRC Cognitive Function and Ageing Study (MRC-CFAS)

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