In the diseased brain, reactive astrocytes are the main cellular source of TIMP-1 (Rivera et al., 1997, 2002; Pagenstecher et al., 1998), which in turn promotes astrocyte proliferation (Ogier et al., 2005; Hernandez-Guillamon et al., 2009), suggesting altogether that TIMP-1 could contribute to AD neuroinflammation and/or downregulate ADAM10 activity. This evidence concerns the gene ADAM10 and Alzheimer disease.