Aβ1-6
Humans
Animals
Mice
Aged
tau Proteins
/ metabolism
Caenorhabditis elegans
/ metabolism
Peptide Fragments
/ metabolism
Amyloid beta-Peptides
/ metabolism
Alzheimer Disease
/ metabolism
Brain
/ metabolism
Brain Injuries, Traumatic
Mice, Transgenic
Disease Models, Animal
Amyloid beta-Protein Precursor
/ metabolism
Journal
Molecular psychiatry
ISSN: 1476-5578
Titre abrégé: Mol Psychiatry
Pays: England
ID NLM: 9607835
Informations de publication
Date de publication:
06 2023
06 2023
Historique:
received:
10
01
2023
accepted:
02
05
2023
revised:
21
04
2023
medline:
30
10
2023
pubmed:
18
5
2023
entrez:
17
5
2023
Statut:
ppublish
Résumé
Alzheimer's disease (AD), the leading cause of dementia in older adults, is a double proteinopathy characterized by amyloid-β (Aβ) and tau pathology. Despite enormous efforts that have been spent in the last decades to find effective therapies, late pharmacological interventions along the course of the disease, inaccurate clinical methodologies in the enrollment of patients, and inadequate biomarkers for evaluating drug efficacy have not allowed the development of an effective therapeutic strategy. The approaches followed so far for developing drugs or antibodies focused solely on targeting Aβ or tau protein. This paper explores the potential therapeutic capacity of an all-D-isomer synthetic peptide limited to the first six amino acids of the N-terminal sequence of the A2V-mutated Aβ, Aβ1-6
Identifiants
pubmed: 37198260
doi: 10.1038/s41380-023-02101-3
pii: 10.1038/s41380-023-02101-3
pmc: PMC10611578
doi:
Substances chimiques
tau Proteins
0
Peptide Fragments
0
Amyloid beta-Peptides
0
Amyloid beta-Protein Precursor
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2433-2444Subventions
Organisme : NIH HHS
ID : P40 OD010440
Pays : United States
Informations de copyright
© 2023. The Author(s).
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