More recently, Capsoni and coworkers postulated that neurodegeneration occurring in a transgenic mouse model of AD is provoked by an imbalance of proNGF/NGF and, consequently, of TrkA/p75 signaling such that the inactivation of TrkA determines a strong cholinergic deficit and AD-like neurodegeneration [117]. The gene discussed is NTRK1; the disease is Alzheimer disease.