Apolipoprotein E ?4 allele is a risk factor for late-onset Alzheimer's disease and vascular dementia in Han Chinese

2001 ◽  
Vol 16 (4) ◽  
pp. 438-439 ◽  
Author(s):  
J. G. Zhang ◽  
J. G. Yang ◽  
Z. X. Lin ◽  
L. He ◽  
G. Y. Feng ◽  
...  
Neurology ◽  
1994 ◽  
Vol 44 (2) ◽  
pp. 342-342 ◽  
Author(s):  
T. Brousseau ◽  
S. Legrain ◽  
C. Berr ◽  
V. Gourlet ◽  
O. Vidal ◽  
...  

2022 ◽  
pp. 0271678X2110690
Author(s):  
Charles E Seaks ◽  
Erica M Weekman ◽  
Tiffany L Sudduth ◽  
Kevin Xie ◽  
Brandi Wasek ◽  
...  

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.


1994 ◽  
Vol 3 (4) ◽  
pp. 569-574 ◽  
Author(s):  
Marie-Christine Chartier-Hariln ◽  
Matthew Parfitt ◽  
Sylvle Legrain ◽  
Jordi Pérez-Tur ◽  
Thierry Brousseau ◽  
...  

2011 ◽  
Vol 7 ◽  
pp. e31-e31
Author(s):  
Claudia Suemoto ◽  
Lea Grinberg ◽  
David Schlesinger ◽  
Jose Farfel ◽  
Renata Leite ◽  
...  

2013 ◽  
Vol 15 (2) ◽  
pp. 279-287 ◽  
Author(s):  
Xiao-Ying Ma ◽  
Jin-Tai Yu ◽  
Wei Wang ◽  
Hui-Fu Wang ◽  
Qiu-Yan Liu ◽  
...  

2014 ◽  
Vol 5 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Sophie Poole ◽  
Sim K Singhrao ◽  
St John Crean

Periodontal disease (PD) is an inflammatory disease affecting tooth-supporting tissues in which interaction of specific bacteria and the host’s immune responses play a pivotal role. The pathogenic bacteria associated with PD are a source of systemic inflammation as they have the ability to enter systemic circulation during everyday tasks such as brushing teeth and chewing food. Alzheimer’s disease (AD) is a form of dementia whereby inflammation is thought to play a key role in its pathogenesis and the risk of developing the disease increasing with age. The exact aetiology of the late-onset AD is unknown but peripheral infections are being considered as a potential risk factor.


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