scholarly journals Apolipoprotein E  4 allele predicted an accelerated rate of cognitive decline in Alzheimer's disease

1999 ◽  
Vol 2 (2) ◽  
pp. 56-56
Author(s):  
D. Burke
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E

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

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

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.

scholarly journals The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Elizabeth R. Tuminello ◽  
S. Duke Han
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Evolutionary Biology ◽  
Future Research ◽  
Antagonistic Pleiotropy ◽  
Life Stages ◽  
New Research ◽  
The Impact

Research on apolipoprotein E (APOE) has consistently revealed a relationship between the gene'sε4 allele and risk for development of Alzheimer's disease (AD). However, research with younger populations ofε4 carriers has suggested that the APOEε4 allele may in fact be beneficial in earlier ages and may only confer risk of cognitive decline later in life. Accordingly, we and others have proposed that APOE may represent an example of antagonistic pleiotropy. Antagonistic pleiotropy is an evolutionary biology concept that proposes certain genes or alleles that may differentially impact fitness during different life stages. We critically review this hypothesis in light of new research of the impact of APOE on cognition and neural integrity across the lifespan. We provide recommendations for the revision of the antagonistic pleiotropy hypothesis of APOE and suggest important avenues for future research in this area.

Differential Cognitive Decline in Alzheimer’s Disease Is Predicted by Changes in Ventricular Size but Moderated by Apolipoprotein E and Pulse Pressure

2021 ◽  
pp. 1-16
Author(s):  
Shraddha Sapkota ◽  
G. Peggy McFall ◽  
Mario Masellis ◽  
Roger A. Dixon ◽  
Sandra E. Black
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Pulse Pressure ◽  
Threshold Effect ◽  
Process Models ◽  
Ventricular Enlargement ◽  
Ventricular Size ◽  
Attention Performance

Background: Differential cognitive trajectories in Alzheimer’s disease (AD) may be predicted by biomarkers from multiple domains. Objective: In a longitudinal sample of AD and AD-related dementias patients (n = 312), we tested whether 1) change in brain morphometry (ventricular enlargement) predicts differential cognitive trajectories, 2) further risk is contributed by genetic (Apolipoprotein E [APOE] ɛ4+) and vascular (pulse pressure [PP]) factors separately, and 3) the genetic + vascular risk moderates this pattern. Methods: We applied a dynamic computational approach (parallel process models) to test both concurrent and change-related associations between predictor (ventricular size) and cognition (executive function [EF]/attention). We then tested these associations as stratified by APOE (ɛ4–/ɛ4+), PP (low/high), and APOE+ PP (low/intermediate/high) risk. Results: First, concurrently, higher ventricular size predicted lower EF/attention performance and, longitudinally, increasing ventricular size predicted steeper EF/attention decline. Second, concurrently, higher ventricular size predicted lower EF/attention performance selectively in APOE ɛ4+ carriers, and longitudinally, increasing ventricular size predicted steeper EF/attention decline selectively in the low PP group. Third, ventricular size and EF/attention associations were absent in the high APOE+ PP risk group both concurrently and longitudinally. Conclusion: As AD progresses, a threshold effect may be present in which ventricular enlargement in the context of exacerbated APOE+ PP risk does not produce further cognitive decline.

Apolipoprotein E: non-cognitive symptoms and cognitive decline in late onset Alzheimer's disease

1997 ◽  
Vol 63 (2) ◽  
pp. 273b-273b ◽  
Author(s):  
C. BALLARD ◽  
H. MASSEY ◽  
H. LAMB ◽  
C. MORRIS; ◽  
C. HOLMES ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Late Onset ◽  
Cognitive Symptoms

Apolipoprotein E genotype does not influence rates of cognitive decline in Alzheimer's disease

Neurology ◽  
1996 ◽  
Vol 47 (2) ◽  
pp. 444-448 ◽  
Author(s):  
J. H. Growdon ◽  
J. J. Locascio ◽  
S. Corkin ◽  
T. Gomez-Isla ◽  
B. T. Hyman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Apolipoprotein E ◽  
Apolipoprotein E Genotype
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