Grimmer T, et al. - In this investigation, researchers analyzed the impact of neprilysin (NEP) on amyloid-β 1-42 (Aβ42) in cerebrospinal fluid (CSF) and on in vivo brain amyloid load with amyloid positron emission tomography (PET) with [¹¹C]PiB (Pittsburgh compound B) and examined correlations with CSF-tau and FDG-PET, biomarkers for neuronal injury. In the same cohort of 23 highly characterized Alzheimer’s disease patients, associations were assessed with global and voxel-based (SPM8) linear regression analyses. Investigators found that CSF-NEP was significantly inversely linked to CSF-Aβ42 and positively 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 is involved in the development of Alzheimer's pathology, among other amyloid clearance mechanisms. Furthermore, the extent and rate of neurodegeneration are associated with CSF-NEP.