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Title: Convergent evidence for mGluR5 in synaptic and neuroinflammatory pathways implicated in ASD.
Austin Authors: Zantomio, Daniela ;Chana, Gursharan;Laskaris, Liliana;Testa, Renee;Everall, Ian;Pantelis, Christos;Skafidas, Efstratios
Affiliation: Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne & Melbourne Health, Parkville, Victoria, Australia
Department of Haematology, Austin Health, Heidelberg, VIC, Australia
The Florey Institute of Neuroscience and Mental Health, Australia
Centre for Neural Engineering, The University of Melbourne, Parkville, Victoria, Australia
Department of Psychiatry, The University of Melbourne, Parkville, Victoria, Australia
Department of Psychology, Monash University, Clayton, Vic, Australia
Centre for Integrative Brain Function, Australia
Issue Date: 19-Feb-2015
Publication information: Neuroscience and Biobehavioral Reviews 2015; 52(): 172-7
Abstract: The pathogenesis of Autism Spectrum Disorder (ASD), a serious neurodevelopmental disorder, is poorly understood. We review evidence for alterations in glutamatergic signalling in the aetiology of ASD, with a focus on the metabotropic glutamate receptor-5 (mGluR5). mGluR5 signalling is important for synapse formation, neuroplasticity and long term potentiation as well as neuroprotection and has been shown to have a regulatory role in neuroinflammation. Evidence for neuroinflammation in ASD is supported by increase in pro-inflammatory cytokines in the blood and cerebrospinal fluid (CSF) and increased number and activation of microglia in postmortem dorsolateral prefrontal cortex (DLPFC). mGlur5 signalling has also been shown to downregulate microglial activation. Therefore, we focus on mGluR5 as a potential unifying explanation for synapse alteration and neuroinflammation seen in ASD. Data from mGluR5 knockout mouse models, and syndromic and non syndromic forms of ASD are discussed in relation to how alterations in mGluR5 are associated with ASD symptoms. This review supports altered mGluR5 functioning as a convergent point in ASD pathogenesis and indicates more research is warranted into mGluR5 as a potential therapeutic target.
Gov't Doc #: 25704074
DOI: 10.1016/j.neubiorev.2015.02.006
Journal: Neuroscience and biobehavioral reviews
Type: Journal Article
Subjects: Autism spectrum disorder
Appears in Collections:Journal articles

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