Mild cognitive impairment: Disparity of incidence and prevalence estimates
ABSTRACT The purpose of conducting this study was to identify areas of concordance and sources of variation for the published rates of prevalence and incidence associated with various definitions for mild cognitive impairment (MCI).
The study used systematic review of studies published in English since 1984. Studies were identified by searching MEDLINE and EMBASE databases. Population-based observational studies of incidence or prevalence of MCI and related terms were eligible for inclusion.
A total of 3,705 citations were identified, and 42 were accepted for inclusion; 35 included data on prevalence and 13 on incidence. The following four terms predominated: age-associated memory impairment (AAMI); cognitive impairment no dementia (CIND); MCI; and amnestic MCI (aMCI). Within each term, the operational definition varied. Substantial variation was observed for both incidence (MCI: 21.5-71.3; aMCI: 8.5-25.9 per 1,000 person-years) and prevalence of each definition of cognitive impairment (AAMI 3.6%-38.4%; CIND 5.1%-35.9%; MCI 3%-42%; aMCI 0.5%-31.9%). CIND and MCI showed increasing prevalence among older age groups, whereas age-specific rates of aMCI were lower and without any apparent age relationship.
Prevalence and incidence estimates associated with MCI vary greatly both between definitions and within a definition across the 42 publications. These wide differences pose a significant challenge to our understanding of the social burden of this disease. Enhancement and standardization of operational definitions of the subtypes of cognitive impairment could improve estimates of disease burden and provide a mechanism to assist in the identification of individuals at risk for future Alzheimer's disease and other dementias.
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ABSTRACT: The relationship between heightened neuroinflammation and cognitive decline in the normally aged brain is still debatable, as most data are derived from insult-related models. Accordingly, the aim of the current study was to determine whether a link could be established for 2 immune markers at the post-transcriptional level; CD68 and MHC-II, in a normally aged (24-month-old) rat population discriminated for their learning abilities. Using the Morris Water Maze (MWM) task, aged rats were divided into aged learning-impaired (AI) or -unimpaired (AU) groups. Western immunoblots of hippocampal tissue revealed a significant increase of CD68 in AI rats compared to the AU group. Moreover, up-regulated CD68 expression correlated with increased latency times in the MWM task. Immunofluorescence for CD68 revealed intense staining in the white matter regions and CA3 subregion of the hippocampus in the AI group. Despite expression of MHC-II in the AI group, no correlation was found. Overall, these data suggest that CD68 could play a role associated with cognitive decline in a subgroup of the normally aged population.Neurobiology of Aging 03/2013; DOI:10.1016/j.neurobiolaging.2013.02.008. · 4.85 Impact Factor
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ABSTRACT: Backgound Identifying mild cognitive impairment (MCI) in midlife could improve early identification of Alzheimer's disease (AD). Also, AD is highly heritable, but the heritability of MCI has not been established. We estimated prevalence rates, association with premorbid general cognitive ability (GCA) and heritability for different definitions of neuropsychologically defined MCI in adults in their 50s.Method We examined 1126 twins aged 51-59 years when recruited into the Vietnam Era Twin Study of Aging (VETSA). Six neurocognitive domains were assessed using tests designed to avoid ceiling effects. To differentiate MCI from low overall ability, criteria included adjustment for GCA measured at approximately age 20 years. As in older adults, prevalence rates varied widely. Among the lower prevalence rates were some definitions of multiple-domain MCI and single-domain amnestic MCI, which may be less likely than other MCI categories to revert to normal on follow-up. Low prevalence rates in middle-aged adults are also more likely to be valid. MCI was also associated with lower premorbid GCA. Heritability estimates for any MCI and amnestic MCI averaged .40-.48. By testing multiple cognitive domains and avoiding ceiling effects, MCI can be identified before age 60 years. Premorbid GCA is a risk/protective factor, but deficits after adjusting for early adult GCA suggest additional processes leading to declining trajectories. Heritabilities were comparable to AD, suggesting MCI as an appropriate phenotype for genetic association studies. Full validation will require follow-up assessments (currently under way). Community-based studies are important for this early identification because adults of this age are unlikely to present in clinics.International Journal of Epidemiology 12/2013; 43(2). DOI:10.1093/ije/dyt242 · 9.20 Impact Factor
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ABSTRACT: Objective In an effort to address earliest detection of Mild Cognitive Impairment (MCI), we examined hippocampal volumes and atrophy in middle-aged males to explore neuroanatomical support for different neuropsychological definitions of MCI. Methods 460 men ages 51-60 underwent neuropsychological testing and an MRI. MCI was defined according to five criteria sets. MRI-derived hippocampal volume and hippocampal occupancy (HOC) were obtained via FreeSurfer. Statistical analyses were performed using linear mixed models. Results Differences in HOC between normal cognitive functioning, amnestic, and non-amnestic MCI were observed using MCI criteria that required one impaired (>1.5 SD) cognitive measure in a given cognitive domain or a cognitive composite score method with a cut-point 2 SD below the mean. Differences in standard hippocampal volume were only found between normal and amnestic presentations and only when using the composite score method. Conclusions Results provide empirical support for detection of pre-MCI in younger cohorts. Convergence of neuropsychological and neuroanatomical data, particularly HOC (as opposed to standard cross-sectional volume), supports early identification of MCI as defined by some neuropsychological criteria.American Journal of Geriatric Psychiatry 08/2014; 23(5). DOI:10.1016/j.jagp.2014.08.011 · 3.52 Impact Factor