Excitotoxicity in the Pathogenesis of Autism

Essa, M. Mohamed; Braidy, Nady; Vijayan, Karthikeyan; Subash, Selvaraju; Guillemin, Gilles J.

doi:10.1007/s12640-012-9354-3

Cited by 86 publications

(55 citation statements)

References 72 publications

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“…Neurodegeneration is an incapacitating multifactorial process affecting one or several neuronal nuclei in the brain, and is characterized by massive loss of neuronal cells [1]. Among the factors involved in neurodegeneration are excitotoxicity, oxidative stress, inflammatory events, mitochondrial dysfunction and energy depletion, protein misfolding and aggregation, damaged cell signaling, apoptosis and necrosis [2–4]. In some cases, such as Huntington’s disease (HD), heritable mutations are responsible for dysfunctional proteins that can trigger deadly cascades, ultimately leading to selective neuronal cell death.…”

Section: Introductionmentioning

confidence: 99%

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

et al. 2015

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The receptor for advanced glycation end products (RAGE) is a pattern-recognition receptor involved in neurodegenerative and inflammatory disorders. RAGE induces cellular signaling upon binding to a variety of ligands. Evidence suggests that RAGE up-regulation is involved in quinolinate (QUIN)-induced toxicity. We investigated the QUIN-induced toxic events associated with early noxious responses, which might be linked to signaling cascades leading to cell death. The extent of early cellular damage caused by this receptor in the rat striatum was characterized by image processing methods. To document the direct interaction between QUIN and RAGE, we determined the binding constant (Kb) of RAGE (VC1 domain) with QUIN through a fluorescence assay. We modeled possible binding sites of QUIN to the VC1 domain for both rat and human RAGE. QUIN was found to bind at multiple sites to the VC1 dimer, each leading to particular mechanistic scenarios for the signaling evoked by QUIN binding, some of which directly alter RAGE oligomerization. This work contributes to the understanding of the phenomenon of RAGE-QUIN recognition, leading to the modulation of RAGE function.

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Section: Introductionmentioning

confidence: 99%

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

et al. 2015

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“…Such a time corresponds to the transformation of oligodendrocytes, migration of neuron precursors from the germinal plate, and the up-regulation of excitatory neurotransmitter pathways. Such factors can be linked to the several neurodevelopmental anomalies noted in ASD (Shinohe et al, 2006; Hughes, 2007; Bassett and Bullmore, 2009; Wegiel et al, 2010; Deoni et al, 2011; Essa et al, 2012). …”

Section: How Could Infection-driven Inflammation Results In Asd? Effecmentioning

confidence: 99%

Autism spectrum disorder in children born preterm—role of exposure to perinatal inflammation

Meldrum¹,

Strunk²,

Currie³

et al. 2013

Front. Neurosci.

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Autism Spectrum Disorder (ASD) is the collective term for neurodevelopmental disorders characterized by qualitative impairments in social interaction, communication, and a restricted range of activities and interests. Many countries, including Australia, have reported a dramatic increase in the number of diagnoses over the past three decades, with current prevalence of ASD at 1 in every 110 individuals (~1%). The potential role for an immune-mediated mechanism in ASD has been implicated by several studies, and some evidence suggests a potential link between prenatal infection-driven inflammation and subsequent development of ASD. Furthermore, a modest number of contemporary studies have reported a markedly increased prevalence of ASD in children born preterm, who are at highest risk of exposure to perinatal inflammation. However, the mechanisms that underpin the susceptibility to infection-driven inflammation during pregnancy and risk of preterm birth, and how these intersect with the subsequent development of ASD in the offspring, is not understood. This review aims to summarize and discuss the potential mechanisms and evidence for the role of prenatal infection on the central nervous system, and how it may increase the susceptibility for ASD pathogenesis in children born preterm.

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“…Disruption of this receptor has been associated with neurological disease including Alzheimer's disease (Hynd et al, 2004;Ong et al, 2013), multiple sclerosis (Kostic et al, 2013), autism (Essa et al, 2013), amyotrophic lateral sclerosis (Guo et al, 2003), and stroke (Hansen, 1995;Choi, 1998;Wang et al, 2010). Although human GLF poisoning cases are primarily from acute exposure, evidence suggests that GLF can produce chronic neurotoxic effects (Calas et al, 2008;Meme et al, 2009) or detrimentally impact the developing brain (Fujii et al, 1996;Watanabe, 1997).…”

Section: Relevance Of In Vitro Results To In Vivo Toxicitymentioning

confidence: 99%

Glufosinate binds N-methyl-d-aspartate receptors and increases neuronal network activity in vitro

et al. 2014

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Excitotoxicity in the Pathogenesis of Autism

Cited by 86 publications

References 72 publications

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

Autism spectrum disorder in children born preterm—role of exposure to perinatal inflammation

Glufosinate binds N-methyl-d-aspartate receptors and increases neuronal network activity in vitro

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