%0 Journal Article
%T APOE ¦Å4, the door to insulin-resistant dyslipidemia and brain fog? A case study
%A Seth Stoykovich
%J Archive of "Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring".
%D 2019
%R 10.1016/j.dadm.2019.01.009
%X For decades, scientists have known that carriers of the apolipoprotein E ¦Å4 (APOE ¦Å4) allele (homozygous/heterozygous) are at respectively higher risk for developing Alzheimer's disease (AD). Although previous research reveals that the APOE ¦Å4 variant impacts the clearance capacity and degradation of ¦Â-amyloid from the brain, as compared with APOE ¦Å3 (wild type with normal risk) and APOE ¦Å2 (variant with accelerated clearance and reduced risk), little has been documented about APOE ¦Å4's dual role in cholesterol transport, both peripheral and cerebral, and the effects of sluggish APOE ¦Å4 cholesterol transport on cerebral metabolic rate. An understanding of the connection between brain metabolism and brain fat/cholesterol transport may unlock new prevention strategies for treating patients with a comorbidity of metabolic syndrome (MetS) with cognitive impairment. Recent findings suggest that the APOE ¦Å4 carrier impedes the shuttling of lipids from neurons and circumvents the storage of fat within the glia lipid droplets. This sluggish transport of lipids to triglyceride droplets in the glia cells can lead to dangerous reactive oxygen species and hydroxyl-free radicals as lipids are prematurely oxidized
%K APOE ¦Å4
%K Alzheimer's disease (AD)
%K Metabolic syndrome (MetS)
%K Type 2 diabetes mellitus (T2DM)
%K Ketogenic diet (KD)
%K Late onset Alzheimer's disease (LOAD)
%K Reactive oxygen species (ROS)
%K Inverse Warburg effect
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423699/