The emerging role of synaptic cell-adhesion pathways in the pathogenesis of autism spectrum disorders (Q22251439)

Europe PubMed Central

title

The emerging role of synaptic cell-adhesion pathways in the pathogenesis of autism spectrum disorders (English)

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autism spectrum disorder

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1

Catalina Betancur

Catalina

Betancur

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PubMed publication ID

7 February 2023

3

Joseph D Buxbaum

Joseph D

Buxbaum

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PubMed publication ID

7 February 2023

Takeshi Sakurai

2

Takeshi

Sakurai

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PubMed publication ID

19541375

7 February 2023

language of work or name

English

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publication date

July 2009

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published in

Trends in Neurosciences

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The new neurobiology of autism: cortex, connectivity, and neuronal organization

volume

32

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issue

7

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page(s)

402-412

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cites work

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Partial reversal of Rett Syndrome-like symptoms in MeCP2 mutant mice

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Dissection of synapse induction by neuroligins: effect of a neuroligin mutation associated with autism

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Nectin: an adhesion molecule involved in formation of synapses

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Juxtaparanodal clustering of Shaker-like K+ channels in myelinated axons depends on Caspr2 and TAG-1

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Disruption of the ProSAP2 gene in a t(12;22)(q24.1;q13.3) is associated with the 22q13.3 deletion syndrome

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X-linked mental retardation and autism are associated with a mutation in the NLGN4 gene, a member of the neuroligin family

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Disruption of contactin 4 (CNTN4) results in developmental delay and other features of 3p deletion syndrome

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3q29 microdeletion syndrome: clinical and molecular characterization of a new syndrome

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Recurrent 16p11.2 microdeletions in autism

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Disruption of the neurexin 1 gene is associated with schizophrenia

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Association analysis of the NrCAM gene in autism and in subsets of families with severe obsessive-compulsive or self-stimulatory behaviors

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Analysis of protocadherin alpha gene deletion variant in bipolar disorder and schizophrenia

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Deletions of VCX-A and NLGN4: a variable phenotype including normal intellect.

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Neuroligin-3-deficient mice: model of a monogenic heritable form of autism with an olfactory deficit.

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Postnatal Neurodevelopmental Disorders: Meeting at the Synapse?

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Control of excitatory and inhibitory synapse formation by neuroligins

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7 January 2021

Reversal of neurological defects in a mouse model of Rett syndrome

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7 January 2021

Strong association of de novo copy number mutations with autism

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7 January 2021

A neuroligin-3 mutation implicated in autism increases inhibitory synaptic transmission in mice

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7 January 2021

Identifying autism loci and genes by tracing recent shared ancestry

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7 January 2021

Novel splice isoforms for NLGN3 and NLGN4 with possible implications in autism

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7 January 2021

Identification of a recurrent breakpoint within the SHANK3 gene in the 22q13.3 deletion syndrome

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A patient with vertebral, cognitive and behavioural abnormalities and a de novo deletion of NRXN1alpha

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Disruption of contactin 4 in three subjects with autism spectrum disorder

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X-linked ichthyosis (steroid sulfatase deficiency) is associated with increased risk of attention deficit hyperactivity disorder, autism and social communication deficits.

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Intranasal insulin to improve developmental delay in children with 22q13 deletion syndrome: an exploratory clinical trial.

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Molecular characterisation of the 22q13 deletion syndrome supports the role of haploinsufficiency of SHANK3/PROSAP2 in the major neurological symptoms

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The postsynaptic architecture of excitatory synapses: a more quantitative view

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Cell-cell signaling during synapse formation in the CNS.

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Cytogenetic abnormalities and fragile-X syndrome in Autism Spectrum Disorder

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Silencing of neuroligin function by postsynaptic neurexins

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7 January 2021

The Arg451Cys-neuroligin-3 mutation associated with autism reveals a defect in protein processing

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Extracellular domains of alpha-neurexins participate in regulating synaptic transmission by selectively affecting N- and P/Q-type Ca2+ channels.

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N-cadherin redistribution during synaptogenesis in hippocampal neurons.

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Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1.

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Shank expression is sufficient to induce functional dendritic spine synapses in aspiny neurons.

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Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice

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Terminal 22q deletion syndrome: a newly recognized cause of speech and language disability in the autism spectrum

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7 January 2021

Neurobehavioral profile and brain imaging study of the 22q13.3 deletion syndrome in childhood

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https://api.crossref.org/works/10.1016%2FJ.TINS.2009.04.003

7 January 2021

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1 reference

https://api.crossref.org/works/10.1016%2FJ.TINS.2009.04.003

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Cell adhesion molecules at the synapse

1 reference

https://api.crossref.org/works/10.1016%2FJ.TINS.2009.04.003

7 January 2021