Open AccessThe relationship between apolipoprotein e4 and bloodbrain barrier dysfunction in Alzheimer Disease
Author(s) -
Vitor Matias Grah,
Guilherme Sampaio Silva,
Karla Viana Rezende,
Ayrton Senna do Brasil Amaral Alves,
Maria Inês Vaz de Oliveira,
Maria Paula Banhara Rodrigues,
Juliana Carollyne Amorim
Publication year - 2021
Language(s) - English
Resource type - Conference proceedings
DOI - 10.5327/1516-3180.091
Subject(s) - apolipoprotein e , blood–brain barrier , disease , pathophysiology , medicine , homeostasis , alzheimer's disease , neuroscience , biology , bioinformatics , central nervous system
Background: Alzheimer disease(AD) is a progressive neurodegenerative dysfunction with a cognitive deficit and amyloid-β(Aβ) accumulation. That said, the apolipoprotein E (ApoE) has 4 variants, with E4 being linked to decreased cerebral blood flow and fragile blood-brain barrier (BBB). In this way, the BBB has an important role in removing substances that are toxic to the brain such as βA protein. Objective: Demonstrate the relationship of ApoE4 and BBB dysfunction in the pathophysiology of AD. Methods: Bibliographic review using the CAPES journals portal, in the last 5 years. Results: After analyzing the studies, it is inferred that in cases of homozygosity for ApoE4 in relation to ApoE3 there is a 15 fold increased chance of developing AD and 3 fold heterozygosity. It is concluded that the mechanism that probably explain is related to the secretion of ApoE by the pericytes that lining brain vessels in the BBB, whilst the subtype E4 exacerbates cyclophilinA, which promotes the activation of metalloproteinase-9, causing junctions rupture between adjacent endothelial cells, promoting the loss of βA homeostasis. Conclusion: It can be inferred, that ApoE has great importance in the regulation of the integrity of BBB’s integrity, is undeniable that such protein has a significant contribution in the pathophysiology of AD, hereupon, it’s urgent that these studies need to be continued to develop new therapies in individuals who express ApoE4.