The possible interplay of synaptic and clock genes in autism spectrum disorders
Open accessAbstract
Autism spectrum disorders (ASD) are complex neurodevelopmental conditions characterized by deficits in social communication, absence or delay in language, and stereotyped and repetitive behaviors. Results from genetic studies reveal one pathway associated with susceptibility to ASD, which includes the synaptic cell adhesion molecules NLGN3, NLGN4, and NRXN1 and a postsynaptic scaffolding protein SHANK3. This protein complex is crucial for the maintenance of functional synapses as well as the adequate balance between neuronal excitation and inhibition. Among the factors that could modulate this pathway are the genes controlling circadian rhythms. Indeed, sleep disorders and low melatonin levels are frequently observed in ASD. In this context, an alteration of both this synaptic pathway and the setting of the clock would greatly increase the risk of ASD. In this chapter, I report genetic and neurobiological findings that highlight the major role of synaptic and clock genes in the susceptibility to ASD. On the basis of these lines of evidence, I propose that future studies of ASD should investigate the circadian modulation of synaptic function as a focus for functional analyses and the development of new therapeutic strategies.
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Sleep and circadian rhythm abnormalities have been implicated in depression and bipolar disorder, attention-deficit disorder, and autism.
“Sleep and circadian rhythm abnormalities in children and adolescents may be risk factors for the development of psychiatric disorders, and have been implicated in depression and bipolar disorder (Harvey et al 2006), attention-deficit disorder (Owens 2008) and autism (Bourgeron 2007).”
From Biological rhythms, higher brain function, and behavior: Gaps, opportunities, and challenges (2009) · cites this paper as Bourgeron 2007
Sleep and circadian rhythm abnormalities in children and adolescents may be risk factors for the development of psychiatric disorders.
“Sleep and circadian rhythm abnormalities in children and adolescents may be risk factors for the development of psychiatric disorders, and have been implicated in depression and bipolar disorder (Harvey et al 2006), attention-deficit disorder (Owens 2008) and autism (Bourgeron 2007).”
From Biological rhythms, higher brain function, and behavior: Gaps, opportunities, and challenges (2009) · cites this paper as Bourgeron 2007
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Self-citation
- Authors
- Bourgeron, T.
- Affiliations
- Institut Pasteur (FR)
- Corresponding author
- Bourgeron, T.
- ORCID
- Bourgeron, T.
- Venue
- Cold Spring Harbor Symposia on Quantitative Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2007-01
- Volume
- 72
- Issue
- 1
- Pages
- 645-654
- ISSN
- 0091-7451 (ISSN-L)
- OpenAlex
- W2118792279
- Cited by
- 185
- References
- 89
- Citations by year
- 2025: 3 · 2024: 11 · 2023: 5 · 2022: 11 · 2021: 20 · 2020: 12 · 2019: 12 · 2018: 4 · 2017: 11 · 2016: 12 · 2015: 13 · 2014: 8 · 2013: 12 · 2012: 11
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Symposia on Quantitative Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Commission
- Institut National de la Santé et de la Recherche Médicale
- Fondation pour la Recherche Médicale
- Fondation de France
- Assistance publique-Hôpitaux de Paris
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- autism spectrum disorder, synaptic genes, clock genes, circadian rhythm, neuroligin-3, NRXN1, SHANK3, synaptic cell adhesion molecules, sleep disorders, melatonin, treatment options
- MeSH terms
- Autistic Disorder, Carrier Proteins, Child, Circadian Rhythm, Female, Humans, Male, Melatonin, Membrane Proteins, Models, Genetic, Models, Neurological, Nerve Tissue Proteins, Sleep Wake Disorders, Synapses, Cell Adhesion Molecules, Neuronal, Neural Cell Adhesion Molecules
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