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Alzheimers Dementia: Lipid species may influence the relationship between APOE and dementia

 Last Update: 2022-03-05
 Source: Internet
 Author: User

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The lipoprotein E (APOE) gene is by far the largest genetic risk factor for sporadic Alzheimer's disease (AD)

There are two alleles of concern: the ε4 allele greatly increases the risk of sporadic AD, while the ε2 allele provides protection or resilience

The ε4 allele greatly increases the risk of sporadic AD, while the ε2 allele provides protection or resilience

Since amyloid beta (Aβ) is at the heart of many hypotheses in the pathogenesis of familial and sporadic AD, the relationship between APOE and sporadic AD has primarily been studied in the context of Aβ accumulation and clearance

As key components of lipoprotein and lipid transport, a logical role for APOE variants in the development of sporadic AD is through perturbation of lipid metabolism

Sporadic AD is a complex disease unique to humans, manifested only by our relatively long lifespan and high cognitive function

Hereby, Tingting Wang et al.

They compared three independent cohorts (the Australian Imaging, Biomarkers and Life>

They found: A total of 237 and 104 lipids were associated with APOE ε2 and ε4, respectively

A total of 237 and 104 lipids were associated with APOE ε2 and ε4, respectively

Lipidome models of individual lipid species or APOE genotypes mediated up to 30% and 10% of APOE ε2 and ε4 treatment effects, respectively

The significance of this study lies in the discovery that plasma lipid species mediates the therapeutic effect of APOE genotype in Alzheimer's disease and thus can be considered as a potential therapeutic target

Plasma lipid species mediate the therapeutic effect of APOE genotype in Alzheimer's disease

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