N-truncated forms of Aβ in CSF, such as Aβ 11–40, Aβ 11–42, Aβ 17–40 and Aβ 17–42, have been suggested to have potential diagnostic value in early AD detection and mild cognitive impairment stratification.36, 37 In contrast to these studies, the present study did not focus on the early AD stage, which is widely considered to be a pivotal time for disease-modifying therapies of AD.38, 39 Our future efforts will focus on determining whether serum and CSF p75NTR-ECD levels are predictors of AD in prodromal or mild cognitive impairment populations. This evidence concerns the gene NGFR and Alzheimer disease.