SwePub
Sök i SwePub databas

  form:Ext_t

Träfflista för sökning "WFRF:(Saykin AJ) "

form:Search_simp_t: WFRF:(Saykin AJ)

  • navigation:Result_t 1-10 navigation:of_t 13
hitlist:Modify_result_t
   
hitlist:Enumeration_thitlist:Reference_thitlist:Reference_picture_thitlist:Find_Mark_t
1.
  •  
2.
  •  
3.
  •  
4.
  •  
5.
  •  
6.
  •  
7.
  •  
8.
  •  
9.
  • Zhou, XP, et al. (creator_code:aut_t)
  • Non-coding variability at the APOE locus contributes to the Alzheimer's risk
  • 2019
  • record:In_t: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10:1, s. 3310-
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Alzheimer’s disease (AD) is a leading cause of mortality in the elderly. While the coding change of APOE-ε4 is a key risk factor for late-onset AD and has been believed to be the only risk factor in the APOE locus, it does not fully explain the risk effect conferred by the locus. Here, we report the identification of AD causal variants in PVRL2 and APOC1 regions in proximity to APOE and define common risk haplotypes independent of APOE-ε4 coding change. These risk haplotypes are associated with changes of AD-related endophenotypes including cognitive performance, and altered expression of APOE and its nearby genes in the human brain and blood. High-throughput genome-wide chromosome conformation capture analysis further supports the roles of these risk haplotypes in modulating chromatin states and gene expression in the brain. Our findings provide compelling evidence for additional risk factors in the APOE locus that contribute to AD pathogenesis.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
  • navigation:Result_t 1-10 navigation:of_t 13

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt tools:Close_t

tools:Permalink_label_t