Longitudinal brain atrophy and CSF biomarkers in early-onset Alzheimer's disease.
Atrophy
Biomarkers
Cerebrospinal fluid
Early-onset Alzheimer's disease
Longitudinal
MRI
Journal
NeuroImage. Clinical
ISSN: 2213-1582
Titre abrégé: Neuroimage Clin
Pays: Netherlands
ID NLM: 101597070
Informations de publication
Date de publication:
2021
2021
Historique:
received:
19
04
2021
revised:
17
08
2021
accepted:
20
08
2021
pubmed:
3
9
2021
medline:
20
1
2022
entrez:
2
9
2021
Statut:
ppublish
Résumé
There is evidence of longitudinal atrophy in posterior brain areas in early-onset Alzheimer's disease (EOAD; aged < 65 years), but no studies have been conducted in an EOAD cohort with fluid biomarkers characterization. We used 3T-MRI and Freesurfer 6.0 to investigate cortical and subcortical gray matter loss at two years in 12 EOAD patients (A + T + N + ) compared to 19 controls (A-T-N-) from the Hospital Clínic Barcelona cohort. We explored group differences in atrophy patterns and we correlated atrophy and baseline CSF-biomarkers levels in EOAD. We replicated the correlation analyses in 14 EOAD (A + T + N + ) and 55 late-onset AD (LOAD; aged ≥ 75 years; A + T + N + ) participants from the Alzheimer's disease Neuroimaging Initiative. We found that EOAD longitudinal atrophy spread with a posterior-to-anterior gradient and beyond hippocampus/amygdala. In EOAD, higher initial CSF NfL levels correlated with higher ventricular volumes at baseline. On the other hand, higher initial CSF Aβ42 levels (within pathological range) predicted higher rates of cortical loss in EOAD. In EOAD and LOAD subjects, higher CSF t-tau values at baseline predicted higher rates of subcortical atrophy. CSF p-tau did not show any significant correlation. In conclusion, posterior cortices, hippocampus and amygdala capture EOAD atrophy from early stages. CSF Aβ42 might predict cortical thinning and t-tau/NfL subcortical atrophy.
Identifiants
pubmed: 34474317
pii: S2213-1582(21)00248-5
doi: 10.1016/j.nicl.2021.102804
pmc: PMC8405839
pii:
doi:
Substances chimiques
Amyloid beta-Peptides
0
Biomarkers
0
tau Proteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
102804Subventions
Organisme : NIA NIH HHS
ID : U01 AG024904
Pays : United States
Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
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