Oral nilotinib, 150 mg and 300 mg, once daily demonstrate a linearly proportional increase to dose in the brain of Alzheimer’s disease (AD) [4] and Parkinson’s disease (PD) [5] patients and reach a CNS concentration (1–5 nM) that directly inhibits DDR1 (IC50 1 nM) [6], thus exhibiting an adequate pharmacokinetics and pharmacodynamics relationship. This evidence concerns the gene DDR1 and early-onset autosomal dominant Alzheimer disease.