Furthermore, a recent large scale proteomics study on capillary microvessels in patients with confirmed capillary CAA, AD and healthy controls showed distinct proteomic profile in CAA cases independent of AD, with microvascular proteome from CAA brain showing enrichment for several proteins as reported in above studies including accumulation of complement C1qb, C1qc, C3 and complement regulator CLU, indicating the role of complement cascade in CAA-associated pathology [197]. The gene discussed is CLU; the disease is Alzheimer disease.