Upregulation of DDRs, including Ddr1, has been observed in post-mortem brains of individuals with AD and Parkinson’s diseases (PD)83, and previous studies show that the inhibition or deletion of Ddr1 can lower toxic proteins such as α-synuclein, tau, and Aβ in AD and PD models, promoting autophagy both in vivo and vitro83,84. This evidence concerns the gene DDR1 and Alzheimer disease.