Brain p3-Alcβ peptide restores neuronal viability impaired by Alzheimer's amyloid β-peptide.
AD therapy
Alzheimer's disease (AD)
PET imaging
alcadein
mitochondria
Journal
EMBO molecular medicine
ISSN: 1757-4684
Titre abrégé: EMBO Mol Med
Pays: England
ID NLM: 101487380
Informations de publication
Date de publication:
08 05 2023
08 05 2023
Historique:
revised:
14
03
2023
received:
16
10
2022
accepted:
14
03
2023
medline:
9
5
2023
pubmed:
31
3
2023
entrez:
30
3
2023
Statut:
ppublish
Résumé
We propose a new therapeutic strategy for Alzheimer's disease (AD). Brain peptide p3-Alcβ37 is generated from the neuronal protein alcadein β through cleavage of γ-secretase, similar to the generation of amyloid β (Aβ) derived from Aβ-protein precursor/APP. Neurotoxicity by Aβ oligomers (Aβo) is the prime cause prior to the loss of brain function in AD. We found that p3-Alcβ37 and its shorter peptide p3-Alcβ9-19 enhanced the mitochondrial activity of neurons and protected neurons against Aβo-induced toxicity. This is due to the suppression of the Aβo-mediated excessive Ca
Identifiants
pubmed: 36994913
doi: 10.15252/emmm.202217052
pmc: PMC10165357
doi:
Substances chimiques
Amyloid beta-Peptides
0
peptide P3
0
Amyloid beta-Protein Precursor
0
Amyloid Precursor Protein Secretases
EC 3.4.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e17052Informations de copyright
© 2023 The Authors. Published under the terms of the CC BY 4.0 license.
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