Grimmer T, Goldhardt O, Yakushev I, et al. - Since neprilysin (NEP) cleaves amyloid-β 1–42 (Aβ42) in the brain, researchers used amyloid positron emission tomography (PET) with [11C]PiB (Pittsburgh compound B) to illustrate the impact of NEP on Aβ42 in cerebrospinal fluid (CSF) and on in vivo amyloid brain load. Furthermore, connections were explored with the neuronal injury biomarkers CSF-tau and FDG-PET. In the same cohort of 23 highly characterized Alzheimer disease patients, associations were calculated using global and voxel-based (SPM8) linear regression analyses. Findings suggested a significant inverse correlation of CSF-NEP with CSF-Aβ42 and a positive correlation with the extent of the neuronal injury as measured by CSF-tau and FDG-PET. CSF-NEP findings are consistent with the premise that local degradation plays a part in the development of Alzheimer pathology, among other amyloid clearance mechanisms. Furthermore, the extent and rate of neurodegeneration are correlated with CSF-NEP.