The role of cell adhesion molecule IgSF9b at the inhibitory synapse and psychiatric disease.
Cell adhesion
Circuit development
Inhibitory synapse
Psychiatric disorders
Schizophrenia
Journal
Neuroscience and biobehavioral reviews
ISSN: 1873-7528
Titre abrégé: Neurosci Biobehav Rev
Pays: United States
ID NLM: 7806090
Informations de publication
Date de publication:
28 Nov 2023
28 Nov 2023
Historique:
received:
06
09
2023
revised:
15
11
2023
accepted:
18
11
2023
medline:
30
11
2023
pubmed:
30
11
2023
entrez:
29
11
2023
Statut:
aheadofprint
Résumé
Understanding perturbations in synaptic function between health and disease states is crucial to the treatment of neuropsychiatric illness. While genome-wide association studies have identified several genetic loci implicated in synaptic dysfunction in disorders such as autism and schizophrenia, many have not been rigorously characterized. Here, we highlight immunoglobulin superfamily member 9b (IgSF9b), a cell adhesion molecule thought to localize exclusively to inhibitory synapses in the brain. While both pre-clinical and clinical studies suggest its association with psychiatric diseases, our understanding of IgSF9b in synaptic maintenance, neural circuits, and behavioral phenotypes remains rudimentary. Moreover, these functions wield undiscovered influences on neurodevelopment. This review evaluates current literature and publicly available gene expression databases to explore the implications of IgSF9b dysfunction in rodents and humans. Through a focused analysis of one high-risk gene locus, we identify areas requiring further investigation and unearth clues related to broader mechanisms contributing to the synaptic etiology of psychiatric disorders.
Identifiants
pubmed: 38029609
pii: S0149-7634(23)00445-1
doi: 10.1016/j.neubiorev.2023.105476
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
105476Informations de copyright
Copyright © 2023 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare no competing financial interests.