Elevated soluble amyloid beta protofibrils in Down syndrome and Alzheimer's disease.
Alzheimer's disease
Amyloid beta
Antibody therapy
Down syndrome
Immunotherapy
Lecanemab
Protofibril
Journal
Molecular and cellular neurosciences
ISSN: 1095-9327
Titre abrégé: Mol Cell Neurosci
Pays: United States
ID NLM: 9100095
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
received:
02
03
2021
revised:
27
05
2021
accepted:
31
05
2021
pubmed:
7
6
2021
medline:
31
12
2021
entrez:
6
6
2021
Statut:
ppublish
Résumé
Down syndrome (DS) is caused by trisomy of chromosome 21, which leads to a propensity to develop amyloid β (Aβ) brain pathology in early adulthood followed later by cognitive and behavioral deterioration. Characterization of the Aβ pathology is important to better understand the clinical deterioration of DS individuals and to identify interventive strategies. Brain samples from people with DS and Alzheimer's disease (AD), as well as non-demented controls (NDC), were analyzed with respect to different Aβ species. Immunohistochemical staining using antibodies towards Aβ was also performed. Elevated levels of soluble Aβ protofibrils and insoluble Aβx-40 and Aβx-42 in formic acid brain extracts, and elevated immunohistochemical staining of Aβ deposits were demonstrated with the antibody BAN2401 (lecanemab) in DS and AD compared with NDC. These data and the promising data in a large phase 2 CE clinical trial with lecanemab suggest that lecanemab may have the potential to preserve cognitive capacity in DS. Lecanemab is currently in a phase 3 CE clinical trial.
Identifiants
pubmed: 34091073
pii: S1044-7431(21)00054-3
doi: 10.1016/j.mcn.2021.103641
pii:
doi:
Substances chimiques
Amyloid
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
103641Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.