The patterns of distribution of CLAC in Aβ plaques were strikingly similar to those in AD brains [18, 27], supporting the notion that the interaction of CLAC with Aβ amyloid modifies the distribution and morphology of Aβ plaques in the brains of double tg mice, and possibly, senile plaques in the brains of patients with AD. This evidence concerns the gene COL25A1 and Alzheimer disease.