Searching for ways out of the autism maze: genetic, epigenetic and environmental clues

Persico, Antonio M.; Bourgeron, Thomas

doi:10.1016/j.tins.2006.05.010

Cited by 575Autism Spectrum Disorder ResearchGenetics and Neurodevelopmental DisordersWilliams Syndrome Research

Searching for ways out of the autism maze: genetic, epigenetic and environmental clues

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Persico, Antonio M., Bourgeron, Thomas·2006·Trends in Neurosciences

DOI 10.1016/j.tins.2006.05.010

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Abstract

Our understanding of human disorders that affect higher cognitive functions has greatly advanced in recent decades, and over 20 genes associated with non-syndromic mental retardation have been identified during the past 15 years. However, proteins encoded by "cognition genes" have such diverse neurodevelopmental functions that delineating specific pathogenetic pathways still poses a tremendous challenge. In this review, we summarize genetic, epigenetic and environmental contributions to neurodevelopmental alterations that either cause or confer vulnerability to autism, a disease primarily affecting social cognition. Taken together, these results begin to provide a unifying view of complex pathogenetic pathways that are likely to lead to autism spectrum disorders through altered neurite morphology, synaptogenesis and cell migration. This review is part of the INMED/TINS special issue "Nature and nurture in brain development and neurological disorders", based on presentations at the annual INMED/TINS symposium (http://inmednet.com/).

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The validity of gene-environment interaction models is supported by known prenatal teratological agents, such as rubella or cytomegalovirus infection, and drugs like thalidomide, misoprostol, and valproic acid, which cause autism only in a subset of presumably vulnerable individuals.
“Finally, the validity of gene-environment interaction models is also supported by known prenatal teratological agents, such as rubella or cytomegalovirus infection, and drugs like thalidomide, misoprostol, and valproic acid, which cause autism only in a subset of presumably vulnerable individuals [230, 233].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [230]
In addition to broader diagnostic criteria and greater awareness, a real increase in incidence is also likely.
“in addition to broader diagnostic criteria and greater awareness, a real increase in incidence is also likely [230, 233].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [230]
Other brain regions in autism display abnormalities generally resulting from reduced programmed cell death and/or increased cell proliferation, altered cell migration, and abnormal cell differentiation with reduced neuronal size and abnormal wiring.
“Other brain regions also display abnormalities generally resulting from reduced programmed cell death and/or increased cell proliferation, altered cell migration, and abnormal cell differentiation with reduced neuronal size and abnormal wiring [118, 230].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [230]
Individuals carrying genetic variants expressing reduced amounts of Reelin and PON1 enzyme, if exposed prenatally to OPs during critical neurodevelopmental periods, could be more likely to suffer from altered neuronal migration resulting in AD.
“Hence individuals carrying genetic variants expressing reduced amounts of Reelin and PON1 enzyme, if exposed prenatally to OPs during critical periods in neurodevelopment, could be more likely to suffer from altered neuronal migration resulting in AD [230].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [230]
Recent investigations into the genetic basis of ASD have suggested that glutamergic and GABA-ergic synapses could be affected.
“However, recent investigations into the genetic basis of ASD have suggested that glutamergic and GABA-ergic synapses could be affected (see Garber, 2007;Persico & Bourgeron, 2006).”
From Vision in autism spectrum disorders (2009) · cites this paper as Persico & Bourgeron, 2006

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Possible Association Between Congenital Cytomegalovirus Infection and Autistic Disorder
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Reelin gene alleles and susceptibility to autism spectrum disorders
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Reelin Is a Serine Protease of the Extracellular Matrix
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The embryonic development of the cerebellum in normal and reeler mutant mice
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Fragile X Mental Retardation Protein (FMRP) Binds Specifically to the Brain Cytoplasmic RNAs BC1/BC200 via a Novel RNA-binding Motif
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The neurobeachin gene is disrupted by a translocation in a patient with idiopathic autism
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Neuroanatomic Variation in Monozygotic Twin Pairs Discordant for the Narrow Phenotype for Autism
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Analysis of IMGSAC autism susceptibility loci: evidence for sex limited and parent of origin specific effects
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NLGN3/NLGN4 gene mutations are not responsible for autism in the Quebec population
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Reelin is a positional signal for the lamination of dentate granule cells
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Analysis of reelin as a candidate gene for autism
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Association of Reelin gene polymorphisms with autism
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Levels of Bcl-2 and P53 Are Altered in Superior Frontal and Cerebellar Cortices of Autistic Subjects
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Reduced Blood Levels of Reelin as a Vulnerability Factor in Pathophysiology of Autistic Disorder
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The Neuropathology of Autism: A Review
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Lack of evidence for an association between WNT2 and RELN polymorphisms and autism
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Alleles of a reelin CGG repeat do not convey liability to autism in a sample from the CPEA network
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Haplotypes in the gene encoding protein kinase c-beta (PRKCB1) on chromosome 16 are associated with autism
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Polymorphic GGC repeat differentially regulates human reelin gene expression levels
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Kinetics of3H-Serotonin uptake by platelets in infantile autism and developmental language disorder (including five pairs of twins)
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Rodier (1996) · doi:10.1002/(sici)1096-9861(19960624)370:2

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Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders
Durand, C. M., Betancur, C., Boeckers, T. M., Bockmann, J., Chaste, P., Fauchereau, F., Nygren, G., Rastam, M., Gillberg, I. C., Anckarsäter, H., et al. (2007) · Nature Genetics · doi:10.1038/ng1933 · Cited by 1,602 · see citing works
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Autism spectrum disorders: developmental disconnection syndromes
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mTOR signaling: At the crossroads of plasticity, memory and disease
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A Neuroligin-3 Mutation Implicated in Autism Increases Inhibitory Synaptic Transmission in Mice
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Consensus Paper: Pathological Role of the Cerebellum in Autism
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Contribution of SHANK3 Mutations to Autism Spectrum Disorder
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The Autistic Neuron: Troubled Translation?
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Autism spectrum disorders and autistic traits: A decade of new twin studies
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Reduced social interaction and ultrasonic communication in a mouse model of monogenic heritable autism
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Abnormal melatonin synthesis in autism spectrum disorders
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The neurobiology of autism
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Abnormal behavior in a chromosome-engineered mouse model for human 15q11-13 duplication seen in autism
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GABAA Receptor Downregulation in Brains of Subjects with Autism
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Genetic and Functional Analyses of SHANK2 Mutations Suggest a Multiple Hit Model of Autism Spectrum Disorders
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Repetitive Self-Grooming Behavior in the BTBR Mouse Model of Autism is Blocked by the mGluR5 Antagonist MPEP
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Sex differences in oxytocin and vasopressin: Implications for autism spectrum disorders?
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AutDB: a gene reference resource for autism research
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Maternal and paternal age and risk of Autism Spectrum Disorders
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A genetic variant that disrupts MET transcription is associated with autism
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The intense world syndrome-an alternative hypothesis for autism
Markram, H. (2007) · Frontiers in Neuroscience · doi:10.3389/neuro.01.1.1.006.2007 · Cited by 394 · see citing works
Immune transcriptome alterations in the temporal cortex of subjects with autism
Garbett, K., Ebert, P. J., Mitchell, A., Lintas, C., Manzi, B., Mirnics, K., & Persico, A. M. (2008) · Neurobiology of Disease · doi:10.1016/j.nbd.2008.01.012 · Cited by 375 · see citing works
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The prevalence of neurodevelopmental disorders in children prenatally exposed to antiepileptic drugs
Bromley, R. L., Mawer, G. E., Briggs, M., Cheyne, C., Clayton-Smith, J., Garcia-Finana, M., Kneen, R., Lucas, S. B., Shallcross, R., Baker, G. A., et al. (2013) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp-2012-304270 · Cited by 367 · see citing works
Autism-like behaviours with transient histone hyperacetylation in mice treated prenatally with valproic acid
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Key role for gene dosage and synaptic homeostasis in autism spectrum disorders
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Oxytocin enhances hippocampal spike transmission by modulating fast-spiking interneurons
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How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis
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Elevated NMDA receptor levels and enhanced postsynaptic long-term potentiation induced by prenatal exposure to valproic acid
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Authors: Persico, A. M., & Bourgeron, T.
Affiliations: Università Campus Bio-Medico (IT)
Institut Pasteur (FR)
Corresponding author: Persico, Antonio M.
ORCID: Persico, Antonio M.
Bourgeron, Thomas
Venue: Trends in Neurosciences
Publisher: Elsevier BV
Published: 2006-07
Volume: 29
Issue: 7
Pages: 349-358
ISSN: 0166-2236 (ISSN-L)
DOI: 10.1016/j.tins.2006.05.010
OpenAlex: W2171804213
Cited by: 575
References: 130
Citations by year: 2026: 3 · 2025: 9 · 2024: 6 · 2023: 9 · 2022: 17 · 2021: 20 · 2020: 17 · 2019: 14 · 2018: 19 · 2017: 24 · 2016: 32 · 2015: 47 · 2014: 40 · 2013: 41 · 2012: 51
FWCI: 3.67
Type: journal article
Language: en
Open access: green
hdl.handle.net
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in Neurosciences (publishedVersion)
PubMed (publishedVersion)
IRIS UNIMORE (University of Modena and Reggio Emilia) (submittedVersion, cc-by)
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 › Developmental Neuroscience › Williams Syndrome Research
Keywords: autism spectrum disorder, autism genetics, epigenetics, environmental risk factors, brain development, intellectual disability, social cognition, synaptogenesis, neurite morphology, neuronal migration, pathogenesis
MeSH terms: Animals, Autistic Disorder, Cell Movement, Disease Models, Animal, Environment, Genetics, Behavioral, Humans, Genetic Linkage, Nerve Tissue Proteins

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Searching for ways out of the autism maze: genetic, epigenetic and environmental clues

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