Causal mediation analysis of the neuroprotection of through lipid pathways.

Background: Recent studies have revealed a strong association between the e2 allele of the Apolipoprotein E ( gene and lipid metabolites. In addition, carriers appear to be protected from cognitive decline and Alzheimer's disease. This correlation supports the hypothesis that lipids may mediate the protective effect of on cognitive function, thereby providing potential targets for therapeutic intervention.

APOE4 and infectious diseases jointly contribute to brain glucose hypometabolism, a biomarker of Alzheimer's pathology: New findings from the ADNI.

Background: Impaired brain glucose metabolism is a preclinical feature of neurodegenerative diseases such as Alzheimer's disease (AD). Infections may promote AD-related pathology. Therefore, we investigated the interplay between infections and APOE4, a strong genetic risk factor for AD.

Metabolite signatures of chronological age, aging, survival, and longevity.

Metabolites that mark aging are not fully known. We analyze 408 plasma metabolites in Long Life Family Study participants to characterize markers of age, aging, extreme longevity, and mortality. We identify 308 metabolites associated with age, 258 metabolites that change over time, 230 metabolites associated with extreme longevity, and 152 metabolites associated with mortality risk.

Elevated blood glucose levels are associated with the progression of brain hypometabolism, and HDL-C and add to this association.

Background: Brain glucose hypometabolism has consistently been found in neurodegenerative disorders, including Alzheimer's disease (AD). High blood glucose and HDL cholesterol (HDL-C) levels have also been linked to neurodegeneration and AD. However, there is limited understanding of the relationships between dementia-related risk factors in the brain and blood.