There is increasing evidence that Alzheimer’s disease not only involves neurons, but also other cell types present in the brain, such as glial cells. Understanding glial cells’ contribution to the pathology therefore promises conceptual advances and, at the same time, offers an important window of opportunity for identifying new therapeutic targets. We recently have shown that patients with Alzheimer’s disease present a disease-dependent increase in the brain expression of a small glial-derived secreted protein named SFRP1, which interacts with harmful amyloid products (the accumulation of which is thought to be among the culprits of the pathology), and down-regulates an enzyme that prevents their generation. Studies in mouse models showed that neutralization of SFRP1 activity counteracts several of the pathological traits of the disease. We now wish to obtain preclinical evidence that this strategy is effective against Alzheimer’s disease progression—and safe, so that treatment will have no relevant side effects. We also will explore whether the presence of SFRP1 in the serum may be predictive of disease progression. We expect this study will provide the necessary information to translate a novel therapeutic target and possibly an additional diagnostic tool for AD to the clinic.