The Role of the Immunoglobulin Superfamily of Cell Adhesion Molecules in Intellectual Disability

16/10/2026

AI Summary

IgSF cell adhesion molecules are essential for axon and dendrite growth, synapse formation, and maturation critical to cognitive function.
Altered levels or functions of IgSF CAMs occur in Fragile X, Rett, Down, autism, L1 syndrome and fetal alcohol disorders, impairing synapse formation.
Functional studies link IgSF CAM dysregulation to learning and behavioural deficits and nominate these molecules as candidate therapeutic targets.

TL;DR (AI Generated)

In this review, we discuss studies showing that levels and functions of IgSF CAMs are affected in various syndromes and disorders associated with intellectual disability, including Fragile X syndrome, Rett syndrome, Down syndrome, autism spectrum disorder, L1 syndrome and fetal alcohol spectrum disorders.

We highlight functional studies in cellular and animal models showing that changes in levels and functions of IgSF CAMs impair synapse formation and induce learning and behavioral abnormalities resembling those found in people with intellectual disability.

Basic summary

Cells. 2026 Oct 2;15(19):1801. doi: 10.3390/cells15191801.

ABSTRACT

Immunoglobulin superfamily (IgSF) cell adhesion molecules (CAMs) are cell surface glycoproteins that play critical roles during multiple stages of synapse formation, including axon and dendrite growth and guidance, target recognition, axo-dendritic contact formation and its maturation into a functional synapse. Intellectual disability is a condition characterized by significant limitations in intellectual functioning and adaptive behaviors. Growing evidence indicates that deficits in synapse formation underlie the pathogenesis of intellectual disability. In this review, we discuss studies showing that levels and functions of IgSF CAMs are affected in various syndromes and disorders associated with intellectual disability, including Fragile X syndrome, Rett syndrome, Down syndrome, autism spectrum disorder, L1 syndrome and fetal alcohol spectrum disorders. We highlight functional studies in cellular and animal models showing that changes in levels and functions of IgSF CAMs impair synapse formation and induce learning and behavioral abnormalities resembling those found in people with intellectual disability. Together, these studies indicate that IgSF CAMs need to be considered as important therapeutic targets for treating intellectual disability and their functions need to be assessed when new treatments of this condition are developed.

PMID:42882499 | DOI:10.3390/cells15191801

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