LAUSR

Tao et al.1 have described an interaction between elevated plasma C-reactive protein (CRP) levels and APOE ε4 burden in data from the Alzheimer's Disease Neuroimaging Initiative (ADNI). They concluded that “CRP released during peripheral inflammation could be a mediator in APOE ε4–related AD neurodegeneration and serve as a drug target for AD.”1 We demonstrated CRP's mediation in data from the Texas Alzheimer's Research and Care Consortium (TARCC), a larger, ethnically diverse, and similarly well-characterized cohort, in 2017.2 The TARCC measures blood-based protein biomarkers in serum by the same methodology and vendor as the ADNI. In our paper, we tested N = 120 serum proteins, and only CRP had an unequivocal mediation effect on the association of APOE with prospectively measured and highly adjusted dementia severity.