Apolipoprotein E ε4 Allele Frequency and Age at Onset of Alzheimer’s Disease

2006 ◽  
Vol 23 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Yvonne Davidson ◽  
Linda Gibbons ◽  
Antonia Pritchard ◽  
Jayne Hardicre ◽  
Joanne Wren ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Allele Frequency ◽  
Age At Onset ◽  
Ε4 Allele

Depression in Alzheimer’s Disease Might Be Associated with Apolipoprotein E ε4 Allele Frequency in Women but Not in Men

2002 ◽  
Vol 14 (2) ◽  
pp. 59-63 ◽  
Author(s):  
Tomas Müller-Thomsen ◽  
Sönke Arlt ◽  
Stefanie Ganzer ◽  
Ulrike Mann ◽  
Reinhard Mass ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Allele Frequency ◽  
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

Apolipoprotein E and Alzheimer's Disease: Strength of Association Is Related to Age at Onset

1996 ◽  
Vol 7 (5) ◽  
pp. 251-255
Author(s):  
D.L. Murman ◽  
N.L. Foster ◽  
S.P. Kilgore ◽  
C.A. McDonagh ◽  
J.K. Fink
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Age At Onset ◽  
Strength Of Association

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.

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

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

Apolipoprotein E ε4/4 genotype limits response to dietary induction of hyperhomocysteinemia and resulting inflammatory signaling

2022 ◽  
pp. 0271678X2110690
Author(s):  
Charles E Seaks ◽  
Erica M Weekman ◽  
Tiffany L Sudduth ◽  
Kevin Xie ◽  
Brandi Wasek ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Apolipoprotein E ◽  
Late Onset ◽  
Apoe Ε4 ◽  
Perivascular Inflammation ◽  
Ε4 Allele ◽  
Barrier Breakdown ◽  
The Impact

Vascular contributions to cognitive impairment and dementia (VCID) are the second leading cause of dementia behind Alzheimer’s disease. Apolipoprotein E (ApoE) is a lipid transporting lipoprotein found within the brain and periphery. The APOE ε4 allele is the strongest genetic risk factor for late onset Alzheimer’s disease and is a risk factor for VCID. Our lab has previously utilized a dietary model of hyperhomocysteinemia (HHcy) to induce VCID pathology and cognitive deficits in mice. This diet induces perivascular inflammation through cumulative oxidative damage leading to glial mediated inflammation and blood brain barrier breakdown. Here, we examine the impact of ApoE ε4 compared to ε3 alleles on the progression of VCID pathology and inflammation in our dietary model of HHcy. We report a significant resistance to HHcy induction in ε4 mice, accompanied by a number of related differences related to homocysteine (Hcy) metabolism and methylation cycle, or 1-C, metabolites. There were also significant differences in inflammatory profiles between ε3 and ε4 mice, as well as significant reduction in Serpina3n, a serine protease inhibitor associated with ApoE ε4, expression in ε4 HHcy mice relative to ε4 controls. Finally, we find evidence of pervasive sex differences within both genotypes in response to HHcy induction.

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