In:
Neurodegenerative Diseases, S. Karger AG, Vol. 19, No. 1 ( 2019), p. 43-50
Abstract:
〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Neprilysin (NEP) cleaves amyloid-β 1–42 (Aβ 〈 sub 〉 42 〈 /sub 〉 ) in the brain. Hence, we aimed to elucidate the effect of NEP on Aβ 〈 sub 〉 42 〈 /sub 〉 in cerebrospinal fluid (CSF) and on in vivo brain amyloid load using amyloid positron emission tomography (PET) with [ 〈 sup 〉 11 〈 /sup 〉 C]PiB (Pittsburgh compound B). In addition, associations with the biomarkers for neuron al injury, CSF-tau and FDG-PET, were investigated. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Associations were calculated using global and voxel-based (SPM8) linear regression analyses in the same cohort of 23 highly characterized Alzheimer’s disease patients. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 CSF-NEP was significantly inversely associated with CSF-Aβ 〈 sub 〉 42 〈 /sub 〉 and positively with the extent of neuronal injury as measured by CSF-tau and FDG-PET. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Our results on CSF-NEP are compatible with the assumption that local degradation, amongst other mechanisms of amyloid clearance, plays a role in the development of Alzheimer’s pathology. In addition, CSF-NEP is associated with the extent and the rate of neurodegeneration.
Type of Medium:
Online Resource
ISSN:
1660-2854
,
1660-2862
Language:
English
Publisher:
S. Karger AG
Publication Date:
2019
detail.hit.zdb_id:
2126858-7
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