scholarly journals Effect of apolipoprotein E ε4 allele on the progression of cognitive decline in the early stage of Alzheimer's disease

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Kazushi Suzuki ◽  
Akihiro Hirakawa ◽  
Ryoko Ihara ◽  
Atsushi Iwata ◽  
Kenji Ishii ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Early Stage ◽  
Ε4 Allele

scholarly journals P2-299: EFFECT OF APOLIPOPROTEIN E ε4 ALLELE ON PROGRESSION RATE OF COGNITIVE DECLINE IN PRODROMAL AND MILD ALZHEIMER'S DISEASE

2019 ◽  
Vol 15 ◽  
pp. P701-P701
Author(s):  
Kazushi Suzuki ◽  
Ryoko Ihara ◽  
Takeshi Ikeuchi ◽  
Atsushi Iwata ◽  
Takeshi Iwatsubo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Progression Rate ◽  
Ε4 Allele

scholarly journals Apolipoprotein E ε4 Allele Is Unrelated to Cognitive or Functional Decline in Alzheimer’s Disease: Retrospective and Prospective Analysis

2006 ◽  
Vol 22 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Timothy Kleiman ◽  
Kristina Zdanys ◽  
Benjamin Black ◽  
Tracy Rightmer ◽  
Monique Grey ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Functional Decline ◽  
Prospective Analysis ◽  
Ε4 Allele

The Role of Apolipoprotein E ε4 in Early and Late Mild Cognitive Impairment

2021 ◽  
Vol 84 (6) ◽  
pp. 472-480
Author(s):  
Yulin Luo ◽  
Li Tan ◽  
Joseph Therriault ◽  
Hua Zhang ◽  
Ying Gao ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Apolipoprotein E ◽  
Amyloid Β ◽  
Disease Assessment ◽  
Tau Pathology ◽  
Ε4 Allele ◽  
State Examination

<b><i>Background:</i></b> Apolipoprotein E (<i>APOE</i>) ε4 is highly associated with mild cognitive impairment (MCI). However, the specific influence of <i>APOE</i> ε4 status on tau pathology and cognitive decline in early MCI (EMCI) and late MCI (LMCI) is poorly understood. Our goal was to evaluate the association of <i>APOE</i> ε4 with cerebrospinal fluid (CSF) tau levels and cognition in EMCI and LMCI patients in the Alzheimer’s Disease Neuroimaging Initiative database, and whether this association was mediated by amyloid-β (Aβ). <b><i>Methods:</i></b> Participants were 269 cognitively normal (CN), 262 EMCI, and 344 LMCI patients. They underwent CSF Aβ42 and tau detection, <i>APOE</i> ε4 genotyping, Mini-Mental State Examination, (MMSE), and Alzheimer’s disease assessment scale (ADAS)-cog assessments. Linear regressions were used to examine the relation of <i>APOE</i> ε4 and CSF tau levels and cognitive scores in persons with and without Aβ deposition (Aβ+ and Aβ−). <b><i>Results:</i></b> The prevalence of <i>APOE</i> ε4 is higher in EMCI and LMCI than in CN (<i>p</i> &#x3c; 0.001 for both), and in LMCI than in EMCI (<i>p</i> = 0.001). <i>APOE</i> ε4 allele was significantly higher in Aβ+ subjects than in Aβ− subjects (<i>p</i> &#x3c; 0.001). Subjects who had a lower CSF Aβ42 level and were <i>APOE</i> ε4-positive experienced higher levels of CSF tau and cognitive scores in EMCI and/or LMCI. <b><i>Conclusions:</i></b> An <i>APOE</i> ε4 allele is associated with increased CSF tau and worse cognition in both EMCI and LMCI, and this association may be mediated by Aβ. We conclude that <i>APOE</i> ε4 may be an important mediator of tau pathology and cognition in the early stages of AD.

Apolipoprotein E and cognitive decline in Alzheimer's disease

Neurology ◽  
1996 ◽  
Vol 47 (2) ◽  
pp. 317-320 ◽  
Author(s):  
B. L. Plassman ◽  
J. C.S. Breitner
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E

Association of Subjective Hearing Loss and Apolipoprotein E ε4 Allele on Alzheimer's Disease Neurodegeneration

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Ryan M. Neff ◽  
Gregory Jicha ◽  
Gregory S. Hawk ◽  
Matthew L. Bush ◽  
Beth McNulty
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hearing Loss ◽  
Apolipoprotein E ◽  
Ε4 Allele

scholarly journals Reduced Hippocampal Insulin-Degrading Enzyme in Late-Onset Alzheimer's Disease Is Associated with the Apolipoprotein E-ε4 Allele

2003 ◽  
Vol 162 (1) ◽  
pp. 313-319 ◽  
Author(s):  
David G. Cook ◽  
James B. Leverenz ◽  
Pamela J. McMillan ◽  
J. Jacob Kulstad ◽  
Sasha Ericksen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Late Onset ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme ◽  
Ε4 Allele

scholarly journals Genetic Effects on Longitudinal Cognitive Decline During the Early Stages of Alzheimer's Disease

2021 ◽  
Author(s):  
Atul Kumar ◽  
Maryam Shoai ◽  
Sebastian Palmqvist ◽  
Erik Stomrud ◽  
John Hardy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Genome Wide Association Study ◽  
Early Stage ◽  
Cognitive Change ◽  
Preclinical Ad ◽  
Genome Wide ◽  
A Genome ◽  
Polygenic Scores

Abstract Background Cognitive decline in early-stage Alzheimer’s disease (AD) may depend on genetic variability. Methods In the Swedish BioFINDER study, we used polygenic scores (PGS) (for AD, intelligence and educational attainment), and genetic variants (in a genome-wide association study [GWAS]) to predict longitudinal cognitive change (measured by MMSE) over a mean of 4.2 years. We included 555 β-amyloid (Aβ) negative cognitively unimpaired (CU) individuals, 206 Aβ-positive CU (preclinical AD), 110 Aβ-negative mild cognitive impairment (MCI) patients, and 146 Aβ-positive MCI patients (prodromal AD). Results Polygenic scores for AD (in Aβ-positive individuals) and intelligence (independent of Aβ-status) were associated with cognitive decline. Eight genes were associated with cognitive decline in GWAS (3 independent of Aβ-status). Conclusions AD risk genes may influence cognitive decline in early AD, while genes related to intelligence may modulate cognitive decline irrespective of disease. Therapies targeting the implicated biological pathways may modulate the clinical course of AD.

scholarly journals A Strategy for Identifying the Risk of Developing Alzheimer's Disease From Healthy Controls: Distance to Novelty Detection Boundary

2020 ◽  
Author(s):  
Jiangbing Mao ◽  
Qinyong Ye ◽  
Hongqing Yang ◽  
Magda Bucholc ◽  
Shuo Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Early Stage ◽  
Novelty Detection ◽  
Imaging Biomarkers ◽  
Support Vector ◽  
Support Vector Data Description ◽  
Healthy Controls

Abstract Background:Machine learning (ML) techniques are expected to tackle the problem of the high prevalence of Alzheimer’s disease (AD) we are facing worldwide. However, few studies of novelty detection (ND), a typical ML technique for safety-critical systems especially in healthcare, were engaged for identifying the risk of developing cognitive impairment from healthy controls (HC) population.Materials and Methods: Two independent datasets were used for this study, including the Australian Imaging Biomarkers and Lifestyle Study of Ageing (AIBL) and the Fujian Medical University Union Hospital (FMUUH), China datasets. Multiple feature selection methods were applied to identify the most relevant features for predicting the severity of AD. Four easily interpretable ND algorithms, including k nearest neighbor, Mixture of Gaussian (MoG), KMEANS, and support vector data description were used to construct predictive models. The models were visualized by drawing their decision boundaries tightly surrounding the HC data. A distance to boundary (DtB) strategy was proposed to differentiate individuals with mild cognitive impairment (MCI) and AD from HC. Results: The best overall MCI&AD detection performance in both AIBL and FMUUH was obtained on the cognitive and functional assessments (CFA) modality only using MoG-based ND with AUC of 0.8757 and 0.9443, respectively. The highest sensitivity of MCI was presented by using a combination of CFA and brain imaging modality. The DTB value reflects the risk of developing cognitive impairment for HC and the dementia severity of MCI/AD.Conclusions: Our findings suggest that applying some non-invasive and cost-effective features can significantly detect cognitive decline in an early stage. The visualized decision boundary and the proposed DtB strategy illustrated the severity of cognitive decline of potential MCI&AD patients in an early stage. The results would help inform future guidelines for developing a clinical decision-making support system aiming at an early diagnosis and prognosis of MCI&AD.

scholarly journals Genetic Effects on Longitudinal Cognitive Decline During the Early Stages of Alzheimer's Disease

2021 ◽  
Author(s):  
Atul Kumar ◽  
Maryam Shoai ◽  
Sebastian Palmqvist ◽  
Erik Stomrud ◽  
John Hardy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Genome Wide Association Study ◽  
Early Stage ◽  
Cognitive Change ◽  
Preclinical Ad ◽  
Genome Wide ◽  
A Genome ◽  
Polygenic Scores

Abstract Background Cognitive decline in early-stage Alzheimer’s disease (AD) may depend on genetic variability. Methods In the Swedish BioFINDER study, we used polygenic scores (PGS) (for AD, intelligence and educational attainment), and genetic variants (in a genome-wide association study [GWAS]) to predict longitudinal cognitive change (measured by MMSE) over a mean of 4.2 years. We included 555 β-amyloid (Aβ) negative cognitively unimpaired (CU) individuals, 206 Aβ-positive CU (preclinical AD), 110 Aβ-negative mild cognitive impairment (MCI) patients, and 146 Aβ-positive MCI patients (prodromal AD). Results Polygenic scores for AD (in Aβ-positive individuals) and intelligence (independent of Aβ-status) were associated with cognitive decline. Eight genes were associated with cognitive decline in GWAS (3 independent of Aβ-status). Conclusions AD risk genes may influence cognitive decline in early AD, while genes related to intelligence may modulate cognitive decline irrespective of disease. Therapies targeting the implicated biological pathways may modulate the clinical course of AD.

A-5 Examining the Interactive Effects of Traumatic Brain Injury and Apolipoprotein E on Cognitive Decline in Alzheimer’s Disease

2021 ◽  
Vol 36 (6) ◽  
pp. 1044-1044
Author(s):  
Claire Alexander ◽  
Julie Suhr
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Negative Impact ◽  
Interactive Effects ◽  
Decline Rate ◽  
History Of ◽  
Positive Effect

Abstract Objective Little research has focused on possible effects of TBI on cognitive decline rate after Alzheimer’s disease (ad) diagnosis. We examined whether Apolipoprotein E (APOE) status and TBI history interact to predict cognitive decline. Method We used data from the National Alzheimer’s Coordinating Centers (N = 463; 42.3% APOE e4 carriers, 7.8% with TBI history, mean baseline age 79.3). Inclusion criteria included normal cognition at baseline with diagnosis of ad at a follow-up visit; baseline age 50 or older; and at least 3 years of follow-up data. Mixed models (random intercept, random slope) were used, with TBI history, APOE status, and their interaction as predictors of interest. Education, race, and history of TIA, stroke, or hypertension were included as covariates. Cognitive measures included mental status exam scores and immediate/delayed story memory. Results After accounting for covariates, TBI history had a positive effect on cognitive decline rate on the screener and immediate memory measures. APOE status did not affect rate of cognitive decline on the screener, but presence of e4 predicted faster decline on immediate and delayed memory. TBI history and APOE status interacted to predict delayed memory decline, such that history of TBI was associated with a reduced rate of decline for e4 non-carriers but there was no effect of TBI for e4 carriers. Conclusion When examining cognitive decline trajectory, TBI history predicted slower decline (a positive effect) while APOE had either a negative impact or no effect, depending on the measure. Future study should examine cognitive decline in the context of demographic and genetic factors.

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