An assessment of the existence of adult neurogenesis in humans and value of its rodent models for neuropsychiatric diseases.
Journal
Molecular psychiatry
ISSN: 1476-5578
Titre abrégé: Mol Psychiatry
Pays: England
ID NLM: 9607835
Informations de publication
Date de publication:
01 2022
01 2022
Historique:
received:
16
07
2021
accepted:
22
09
2021
revised:
08
09
2021
pubmed:
21
10
2021
medline:
5
4
2022
entrez:
20
10
2021
Statut:
ppublish
Résumé
In sub-mammalian vertebrates like fishes, amphibians, and reptiles, new neurons are produced during the entire lifespan. This capacity diminishes considerably in birds and even more in mammals where it persists only in the olfactory system and hippocampal dentate gyrus. Adult neurogenesis declines even more drastically in nonhuman primates and recent evidence shows that this is basically extinct in humans. Why should such seemingly useful capacity diminish during primate evolution? It has been proposed that this occurs because of the need to retain acquired complex knowledge in stable populations of neurons and their synaptic connections during many decades of human life. In this review, we will assess critically the claim of significant adult neurogenesis in humans and show how current evidence strongly indicates that humans lack this trait. In addition, we will discuss the allegation of many rodent studies that adult neurogenesis is involved in psychiatric diseases and that it is a potential mechanism for human neuron replacement and regeneration. We argue that these reports, which usually neglect significant structural and functional species-specific differences, mislead the general population into believing that there might be a cure for a variety of neuropsychiatric diseases as well as stroke and brain trauma by genesis of new neurons and their incorporation into existing synaptic circuitry.
Identifiants
pubmed: 34667259
doi: 10.1038/s41380-021-01314-8
pii: 10.1038/s41380-021-01314-8
pmc: PMC8967762
mid: NIHMS1768709
doi:
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
377-382Subventions
Organisme : NIMH NIH HHS
ID : R01 MH113257
Pays : United States
Organisme : NIDA NIH HHS
ID : R37 DA023999
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA023999
Pays : United States
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature Limited.
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