Effects of education on the progression of early- versus late-stage mild cognitive impairment

2012 ◽  
Vol 25 (4) ◽  
pp. 597-606 ◽  
Author(s):  
Byoung Seok Ye ◽  
Sang Won Seo ◽  
Hanna Cho ◽  
Seong Yoon Kim ◽  
Jung-Sun Lee ◽  
...  

ABSTRACTBackground: Highly educated participants with normal cognition show lower incidence of Alzheimer's disease (AD) than poorly educated participants, whereas longitudinal studies involving AD have reported that higher education is associated with more rapid cognitive decline. We aimed to evaluate whether highly educated amnestic mild cognitive impairment (aMCI) participants show more rapid cognitive decline than those with lower levels of education.Methods: A total of 249 aMCI patients enrolled from 31 memory clinics using the standard assessment and diagnostic processes were followed with neuropsychological evaluation (duration 17.2 ± 8.8 months). According to baseline performances on memory tests, participants were divided into early-stage aMCI (−1.5 to −1.0 standard deviation (SD)) and late-stage aMCI (below −1.5 SD) groups. Risk of AD conversion and changes in neuropsychological performances according to the level of education were evaluated.Results: Sixty-two patients converted to AD over a mean follow-up of 1.43 years. The risk of AD conversion was higher in late-stage aMCI than early-stage aMCI. Cox proportional hazard models showed that aMCI participants, and late-stage aMCI participants in particular, with higher levels of education had a higher risk of AD conversion than those with lower levels of education. Late-stage aMCI participants with higher education showed faster cognitive decline in language, memory, and Clinical Dementia Rating Sum of Boxes (CDR-SOB) scores. On the contrary, early-stage aMCI participants with higher education showed slower cognitive decline in MMSE and CDR-SOB scores.Conclusions: Our findings suggest that the protective effects of education against cognitive decline remain in early-stage aMCI and disappear in late-stage aMCI.

2012 ◽  
Vol 8 (4S_Part_9) ◽  
pp. P329-P330
Author(s):  
Byoung Seok Ye ◽  
Geon Ha Kim ◽  
Hanna Cho ◽  
Ji Soo Shin ◽  
Young Noh ◽  
...  

Author(s):  
A.J. Sinclair ◽  
B. Vellas

The recent addition of the Diabetes and Cognitive Decline section to JPAD marks a milestone in the history of this progressive journal as it recognises the important contribution that Diabetes makes to the aetiology of both vascular and neurodegenerative dementia syndromes (1-3). It has been observed that diabetes in the presence of hypertension leads to a more pronounced cognitive decline (4) and that at an early stage of cognitive decline (mild cognitive impairment ( MCI)), diabetes accelerates the progression of MCI to dementia (5).


2018 ◽  
Author(s):  
Jeremy A. Elman ◽  
Matthew S. Panizzon ◽  
Mark W. Logue ◽  
Nathan A. Gillespie ◽  
Michael C. Neale ◽  
...  

ABSTRACTBACKGROUNDAlzheimer’s disease (AD) is under considerable genetic influence. However, known susceptibility loci only explain a modest proportion of variance in disease outcomes. This small proportion could occur if the etiology of AD is heterogeneous. We previously found that an AD polygenic risk score (PRS) was significantly associated with mild cognitive impairment (MCI), an early stage of AD. Poor cardiovascular health is also associated with increased risk for AD and has been found to interact with AD pathology. Conditions such as coronary artery disease (CAD) are also heritable, and may contribute to heterogeneity if there are interactions of genetic risk for these conditions as there is phenotypically. However, case-control designs based on prevalent cases of a disease with relatively high case-fatality rate such as CAD may be biased toward individuals who have long post-event survival times and may therefore also identify loci with protective effects.METHODSWe compared interactions between an AD-PRS and two CAD-PRSs, one based on a GWAS of incident cases and one on prevalent cases, on MCI status in 1,209 individuals.RESULTSAs expected, the incidence-based CAD-PRS interacts with the AD-PRS to further increase MCI risk. Conversely, higher prevalence-based CAD-PRSs reduced the effect of AD genetic risk on MCI status.CONCLUSIONSThese results demonstrate: i) the utility of including multiple PRSs and their interaction effects; ii) how genetic risk for one disease may modify the impact of genetic risk for another; and iii) the importance of considering ascertainment procedures of GWAS being used for genetic risk prediction.


Author(s):  
Panteleimon Giannakopoulos ◽  
Pascal Missonnier ◽  
Enikö Kövari ◽  
Gabriel Gold ◽  
Agnès Michon

Author(s):  
Mari Kasai ◽  
Tomohiro Sugawara ◽  
Junko Takada ◽  
Keiichi Kumai ◽  
Kei Nakamura ◽  
...  

Introduction: To assess cognitive impairment, self-awareness is an important issue. The Ascertain Dementia 8 questionnaire (AD8) is a brief observation checklist for detecting mild cognitive impairment (MCI) and dementia. After analyzing the reliability and validity of a self-reported Japanese version of the AD8 (AD8-J), we compared self- and informant-reported versions of the AD8-J. Methods: A total of 93 community residents aged 75 years or older living in Wakuya, Northern Japan, agreed to participate in this study; 35 were rated as Clinical Dementia Rating (CDR) 0 (healthy), 46 as CDR 0.5 (defined herein as MCI), and 12 as CDR 1 or above (dementia, confirmed by the DSM-IV). We examined the reliability and validity using a receiver operating characteristic (ROC) curve. We analyzed the differences between self-reported and informant-reported AD8-J using a repeated measures ANOVA. Results: The self-reported AD8-J showed a satisfactory reliability (i.e., Cronbach coefficient, α = 0.71; Guttman split half method coefficient = 0.60). For CDR 0 vs. CDR 0.5 or above, the area under the ROC curve was 0.74 and the cutoff score was 1/2, with a sensitivity of 70.7% and a specificity of 65.7%. Analysis of the subscores of AD8 suggested that, from the early stage of dementia, the subjects showed a subjective decline in memory and interest in hobbies/activities, as well as problems with judgment. Conclusion: It is suggested that the self-reported AD8-J was effective in detecting MCI and dementia. We could use it for detecting MCI and dementia, including in those living alone, in the primary health checkup.


2021 ◽  
Vol 13 ◽  
Author(s):  
Yu-Wan Yang ◽  
Kai-Cheng Hsu ◽  
Cheng-Yu Wei ◽  
Ray-Chang Tzeng ◽  
Pai-Yi Chiu

Objectives: The Clinical Dementia Rating (CDR) Scale is the gold standard for the staging of dementia due to Alzheimer's disease (AD). However, the application of CDR for the staging of subjective cognitive decline (SCD) and mild cognitive impairment (MCI) in AD remains controversial. This study aimed to use the sum of boxes of the CDR (CDR-SB) plus an SCD single questionnaire to operationally determine the different stages of cognitive impairment (CI) due to AD and non-AD.Methods: This was a two-phase study, and we retrospectively analyzed the Show Chwan Dementia registry database using the data selected from 2015 to 2020. Individuals with normal cognition (NC), SCD, MCI, and mild dementia (MD) due to AD or non-AD with a CDR < 2 were included in the analysis.Results: A total of 6,946 individuals were studied, including 875, 1,009, 1,585, and 3,447 with NC, SCD, MCI, and MD, respectively. The cutoff scores of CDR-SB for NC/SCD, SCD/MCI, and MCI/dementia were 0/0.5, 0.5/1.0, and 2.5/3.0, respectively. The receiver operating characteristic (ROC) analysis showed that the area under the curve (AUC) values of the test groups were 0.85, 0.90, and 0.92 for discriminating NC from SCD, SCD from MCI, and MCI from dementia, respectively. Compared with the Cognitive Abilities Screening Instrument or the Montreal Cognitive Assessment, the use of CDR-SB is less influenced by age and education.Conclusion: Our study showed that the operational determination of SCD, MCI, and dementia using the CDR-SB is practical and can be applied in clinical settings and research on CI or dementia.


BMJ Open ◽  
2019 ◽  
Vol 9 (5) ◽  
pp. e028441
Author(s):  
Melanie Bayly ◽  
Debra Morgan ◽  
Julie Kosteniuk ◽  
Valerie Elliot ◽  
Amanda Froehlich Chow ◽  
...  

IntroductionCaregivers of persons with dementia and mild cognitive impairment (MCI) are at risk of decreased well-being. While many interventions for caregivers exist, evidence is sparse regarding intervention timing and effectiveness at an early stage of cognitive decline. Our systematic review aims to answer the following questions: (1) Do interventions for caregivers of persons with early stage dementia or MCI affect their well-being and ability to provide care? (2) Are particular types of caregiver interventions most effective during early stage cognitive decline? (3) How does effectiveness differ when early and later interventions are directly compared? (4) Do effects of early stage caregiver intervention vary based on care recipient and caregiver characteristics (eg, sex, type of dementia)?Methods and analysisThe databases MEDLINE, EMBASE, PSYCINFO and CINAHL, as well as grey literature databases, will be searched for English language studies using search terms related to caregiver interventions and dementia/MCI. Abstracts and full texts will be screened by two independent reviewers; included studies must assess the effects of an intervention for caregivers of persons with early stage dementia or MCI on caregiver well-being or ability to provide care. Intervention, study and participant characteristics will be extracted by two independent reviewers, along with outcome data. Risk of bias will be assessed using the Cochrane risk of bias tool (for controlled trials with and without randomisation). Interventions will be grouped by type (eg, psychoeducational) and a narrative synthesis is planned due to expected heterogeneity, but a meta-analysis will be performed where possible. The Grading of Recommendations, Assessment, Development and Evaluations approach will be used to inform conclusions regarding the quality of evidence for each type of intervention.Ethics and disseminationFindings from this review will be disseminated via conferences and peer-reviewed publication, and a summary will be provided to the Alzheimer Society.PROSPERO registration numberCRD42018114960.


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