However, neprilysin is only able to degrade soluble forms of Aβ; thus, once the insoluble Aβ forms, such as fibrils, are present, the role of glial cells and matrix metalloporteases, such as MMP-1, -2 and -9, is fundamental and, as has been demonstrated systematically, alterations in glial response as well as an altered activity of MMPs could be well related to neurodegeneration and AD (Mroczko et al., 2013; Table 1). The gene discussed is MME; the disease is Alzheimer disease.