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Plasma β‐secretase1 concentrations correlate with basal forebrain atrophy and neurodegeneration in cognitively healthy individuals at risk for AD
Author(s) -
Vergallo Andrea,
Lemercier Pablo,
Cavedo Enrica,
Lista Simone,
Vanmechelen Eugeen,
De Vos Ann,
Zetterberg Henrik,
Blennow Kaj,
Habert MarieOdile,
Potier MarieClaude,
Dubois Bruno,
Teipel Stefan,
Hampel Harald
Publication year - 2021
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.12228
Subject(s) - neurodegeneration , biomarker , hippocampus , atrophy , entorhinal cortex , basal forebrain , medicine , psychology , alzheimer's disease , endocrinology , standardized uptake value , neuroscience , positron emission tomography , pathology , disease , chemistry , central nervous system , biochemistry
Background Increased β‐secretase 1 (BACE1) protein concentration, in body fluids, is a candidate biomarker of Alzheimer's disease (AD).We reported that plasma BACE1 protein concentrations are associated with the levels of brain amyloidβ (Αβ) accumulation in cognitively healthy individuals with subjective memory complaint (SMC). Methods In 302 individuals from the same cohort, we investigated the cross‐sectional and longitudinal association between plasma BACE1 protein concentrations and AD biomarkers of neurodegeneration (plasma t‐tau and Neurofilament light chain (NfL), fluorodeoxyglucose–positron emission tomography (FDG‐PET), brain volumes in the basal forebrain [BF], hippocampus, and entorhinal cortex). Results We report a positive longitudinal correlation of BACE1 with both NfL and t‐tau, as well as a correlation between annual BACE1 changes and bi‐annual reduction of BF volume. We show a positive association between BACE1 and FDG‐PET signal at baseline. Conclusions The association between plasma BACE1 protein concentrations and BF atrophy we found in cognitively healthy individuals with SMC corroborates translational studies, suggesting a role of BACE1 in neurodegeneration.