In individuals with Alzheimer's disease (AD), peripheral inflammation escalates amyloid beta levels in the brain,[25] potentially due to increased blood‐to‐brain influx and decreased brain‐to‐blood efflux across the blood‐brain barrier.[26] Subsequently, it can foster neuroinflammation and disease advancement.[27] While treating the brain organoid with the at‐risk and HC‐like plasma, the only protein significantly upregulated with FDR<0.05 in at‐risk plasma‐treated organoid was CXCL4 when compared to the HC‐like plasma. This evidence concerns the gene PF4 and Alzheimer disease.