Topic
Cognitive decline
About: Cognitive decline is a research topic. Over the lifetime, 29308 publications have been published within this topic receiving 1174689 citations.
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TL;DR: It is indicated that few social ties, poor integration, and social disengagement are risk factors for cognitive decline among community-dwelling elderly persons.
Abstract: Objectives. To examine the influence of social networks and social engagement on cognitive decline in a population-based cohort of elderly people, and to assess gender differences in the effect of social relations on cognition.
Methods. A longitudinal study of community-dwelling people over 65 was carried out. Cognitive function (orientation and memory) in 1997 and cognitive decline (absent, mild, and severe) over 4 years (1993–1997) were assessed using an instrument previously validated for populations with a low level of education. The effect of social networks, social integration, and social engagement with friends, children, and relatives on cognitive function and cognitive decline was estimated by multiple linear and logistic regressions after adjusting for age, sex, education, depressive symptoms, systolic and diastolic blood pressure, and functional status.
Results. Poor social connections, infrequent participation in social activities, and social disengagement predict the risk of cognitive decline in elderly individuals. The probability of cognitive decline was lower for both men and women with a high frequency of visual contact with relatives and community social integration. Engagement with friends seemed to be protective for cognitive decline in women but not in men.
Discussion. This longitudinal study indicates that few social ties, poor integration, and social disengagement are risk factors for cognitive decline among community-dwelling elderly persons. The nature of the ties that influence cognition may vary in men and women.
622 citations
TL;DR: Small infarcts in AD patients have no essential impact on global cognitive decline which mainly depends on the severity of Alzheimer pathology, but in early stage of AD they may influence and promote the development of dementia.
Abstract: Recent epidemiological and clinico-pathologic data suggest overlaps between Alzheimer disease (AD) and cerebrovascular lesions that may magnify the effect of mild AD pathology and promote progression of cognitive decline or even may precede neuronal damage and dementia. Vascular pathology in the aging brain and in AD includes: 1. cerebral amyloid angiopathy (CAA) with an incidence of 82-98% often associated with ApoE epsilon 2 and causing a) cerebral mass hemorrhages (around 70%, mainly in the frontal and parietal lobes), b) multiple or recurrent microhemorrhages (15%), and c) ischemic (micro-)infarcts or lacunes (around 20%). The frequency of these lesions increases with the severity of CAA and shows no correlation with that of senile amyloid plaques. CAA, significantly more frequent in patients with cerebral hemorrhages or infarcts than in aged controls, is an important risk factor for cerebrovascular lesions in AD. 2. Microvascular changes with decreased density and structural abnormalities causing regional metabolic and blood-brain barrier dysfunctions with ensuing neuronal damage. In large autopsy series of demented aged subjects, around 80% show Alzheimer type pathology, 20-40% with additional, often minor vascular lesions, 7-10% "pure" vascular dementia, and 3-5% "mixed" dementia (combination of AD and vascular encephalopathy). AD cases with additional minor cerebrovascular lesions have significantly more frequent histories of hypertension or infarcts than "pure" AD patients. Vascular lesions in AD include cortical microinfarcts, subcortical lacunes, white matter lesions / leukoencephalopathy, small hemorrhages and corticosubcortical infarcts, while in mixed type dementia multiple larger or hemispheral infarcts are more frequent. Small infarcts in AD patients have no essential impact on global cognitive decline which mainly depends on the severity of Alzheimer pathology, but in early stage of AD they may influence and promote the development of dementia. Recent studies showed lower density of plaques and tangles in brains with cerebrovascular lesions, and similar severity of dementia was related to fewer AD lesions in brains with than in those without small vascular lesions. Further studies will help to elucidate the risk factors and impact of cerebrovascular lesions on the development and progression of dementia in AD.
620 citations
TL;DR: A new secondary prevention trial in older people with amyloid accumulation at high risk for Alzheimer’s disease dementia should provide insights into whether anti-amyloid therapy can delay cognitive decline.
Abstract: A new secondary prevention trial in older people with amyloid accumulation at high risk for Alzheimer's disease dementia should provide insights into whether anti-amyloid therapy can delay cognitive decline.
617 citations
TL;DR: It is suggested that an EC stage of brain involvement can be detected in normal elderly that predicts future cognitive and brain metabolism reductions and Progressive E4-related hypometabolism may underlie the known increased susceptibility for dementia.
Abstract: Neuropathology studies show that patients with mild cognitive impairment (MCI) and Alzheimer’s disease typically have lesions of the entorhinal cortex (EC), hippocampus (Hip), and temporal neocortex. Related observations with in vivo imaging have enabled the prediction of dementia from MCI. Although individuals with normal cognition may have focal EC lesions, this anatomy has not been studied as a predictor of cognitive decline and brain change. The objective of this MRI-guided 2-[18F]fluoro-2-deoxy-D-glucosey positron-emission tomography (FDGyPET) study was to examine the hypothesis that among normal elderly subjects, EC METglu reductions predict decline and the involvement of the Hip and neocortex. In a 3-year longitudinal study of 48 healthy normal elderly, 12 individuals (mean age 72) demonstrated cognitive decline (11 to MCI and 1 to Alzheimer’s disease). Nondeclining controls were matched on apolipoprotein E genotype, age, education, and gender. At baseline, metabolic reductions in the EC accurately predicted the conversion from normal to MCI. Among those who declined, the baseline EC predicted longitudinal memory and temporal neocortex metabolic reductions. At follow-up, those who declined showed memory impairment and hypometabolism in temporal lobe neocortex and Hip. Among those subjects who declined, apolipoprotein E E4 carriers showed marked longitudinal temporal neocortex reductions. In summary, these data suggest that an EC stage of brain involvement can be detected in normal elderly that predicts future cognitive and brain metabolism reductions. Progressive E4-related hypometabolism may underlie the known increased susceptibility for dementia. Further study is required to estimate individual risks and to determine the physiologic basis for METglu changes detected while cognition is normal.
615 citations
TL;DR: Few potentially beneficial factors were identified from the evidence on risk or protective factors associated with cognitive decline, but the overall quality of the evidence was low.
Abstract: Based on an evidence review conducted to support the National Institutes of Health's State-of-the-Science Conference, this systematic review summarizes evidence about putative risk and protective f...
614 citations