Biomarkers

Area of Science:

• Neuroscience
• Immunology
• Genetics

Background:

• Peripheral inflammation is a known risk factor for Alzheimer's disease (AD) development and progression.
• Aging increases inflammation, potentially preceding AD onset.
• A parental history of AD increases an individual's lifetime risk for the disease.

Purpose of the Study:

• To investigate if a parental history of AD is associated with increased peripheral inflammation in middle-aged adults.
• To determine if individuals with a parental history of AD exhibit higher levels of pro-inflammatory cytokines compared to those without.
• To examine these associations across diverse racial and ethnic groups.

Main Methods:

• Analysis of 1,043 non-Hispanic White, non-Hispanic Black, and Hispanic adults from the Offspring Study.
• Determination of parental AD status via a diagnostic consensus conference.
• Measurement of plasma chemokine and cytokine concentrations using Luminex technology, with adjustments for age, sex, race, ethnicity, and APOE genotype.

Main Results:

• Participants with a parental history of AD showed higher levels of Eotaxin and lower levels of G-CSF, VEGF-A, and IL-27.
• Specific differences observed: IL-18 higher in Black individuals, EGF higher in White individuals with parental AD history.
• Women with a parental history of AD had elevated levels of IFna2, IL-12p70, sCD40L, and IL-18.

Conclusions:

• A parental history of Alzheimer's disease is associated with elevated peripheral inflammation markers.
• The observed associations between parental AD history and inflammation vary significantly by sex and race/ethnicity.
• These findings highlight potential inflammatory pathways influenced by genetics and demographics in AD risk.