This apparent inconsistency at 6 months could reflect adaptive mechanisms (e.g., increased turnover of TIMP-1) set in motion to keep the levels of TIMP-1 within a physiological range, and therefore prevent for instance excessive inhibition of metalloproteinases presumably involved in AD homeostatic responses; α-secretase ADAM-10 and Aβ-degrading enzymes MMP-2 and MMP-9 are paradigmatic examples of TIMP-1 targets (Rivera et al., 2010). This evidence concerns the gene MMP2 and Alzheimer disease.