Exploring potential developmental origins of common neurodegenerative disorders.
aging
neurodegeneration
neurodevelopment
signalling
stem cells
Journal
Biochemical Society transactions
ISSN: 1470-8752
Titre abrégé: Biochem Soc Trans
Pays: England
ID NLM: 7506897
Informations de publication
Date de publication:
25 Apr 2024
25 Apr 2024
Historique:
received:
11
09
2023
revised:
12
03
2024
accepted:
11
04
2024
medline:
25
4
2024
pubmed:
25
4
2024
entrez:
25
4
2024
Statut:
aheadofprint
Résumé
In the United States, it is now estimated that 6.7 million people over the age of 65 are afflicted by Alzheimer's disease (AD), over 1 million people are living with Parkinson's disease (PD), and over 200 000 have or are at risk for developing Huntington's disease (HD). All three of these neurodegenerative diseases result in the ultimate death of distinct neuronal subtypes, and it is widely thought that age-related damage is the single biggest contributing factor to this neuronal death. However, recent studies are now suggesting that developmental defects during early neurogenesis could also play a role in the pathology of neurodegenerative diseases. Loss or overexpression of proteins associated with HD, PD, and AD also result in embryonic phenotypes but whether these developmental defects slowly unmask over time and contribute to age-related neurodegeneration remains highly debated. Here, we discuss known links between embryonic neurogenesis and neurodegenerative disorders (including common signaling pathways), potential compensatory mechanisms that could delay presentation of neurodegenerative disorders, and the types of model systems that could be used to study these links in vivo.
Identifiants
pubmed: 38661189
pii: 234369
doi: 10.1042/BST20230422
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2024 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.