Proteomic studies in white matter or isolated amyloid-laden blood vessels from CAA donors showed enrichment in the terminal pathway regulator clusterin, suggesting a compensatory mechanism to limit MAC formation [98,99]; in contrast, genetic ablation of clusterin in AD mice reduced amyloid load and brain inflammation by causing redistribution of amyloid from plaques to the perivascular compartment [100]. This evidence concerns the gene CLU and amyloidosis.