2017
DOI: 10.1016/j.jpsychires.2016.09.003
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Initial analysis of peripheral lymphocytic extracellular signal related kinase activation in autism

Abstract: Background Dysregulation of extracellular signal-related kinase (ERK) activity has been potentially implicated in the pathophysiology of autistic disorder (autism). ERK is part of a central intracellular signaling cascade responsible for a myriad of cellular functions. ERK is expressed in peripheral blood lymphocytes, and measurement of activated (phosphorylated) lymphocytic ERK is commonly executed in many areas of medicine. We sought to conduct the first study of ERK activation in humans with autism by utili… Show more

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Cited by 6 publications
(4 citation statements)
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“…Fourth, although we assessed biological measures that had been previously implicated in prosocial behavior, ASD, and/or ASD-related syndromes, we did not observe relationships between CSF OXT concentration or blood kinase signaling and social trait variation here. This is in contrast to prior research in humans that has linked neonatal CSF OXT concentration to later social engagement [73], and blood kinase signaling to ASD and its symptom severity [74][75][76]. However, absence of evidence implicating these biological measures in monkey social functioning is not necessarily evidence of absence.…”
Section: Limitationscontrasting
confidence: 65%
“…Fourth, although we assessed biological measures that had been previously implicated in prosocial behavior, ASD, and/or ASD-related syndromes, we did not observe relationships between CSF OXT concentration or blood kinase signaling and social trait variation here. This is in contrast to prior research in humans that has linked neonatal CSF OXT concentration to later social engagement [73], and blood kinase signaling to ASD and its symptom severity [74][75][76]. However, absence of evidence implicating these biological measures in monkey social functioning is not necessarily evidence of absence.…”
Section: Limitationscontrasting
confidence: 65%
“…A further, conceptual limitation is that our animal models (except BTBR T+tf/J mice) are based on specific etiological factors, and do not model idiopathic ASD as such. However, there are no animal models of idiopathic ASD in this sense, as even BTBR T+tf/J mice were reported to share some genetic features with clinical ASD 76 78 . Our hypothesis was that individuals with ASD and rodent models of ASD may share key pathophysiological mechanisms regardless of etiology 79 .…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, ERK-related mutations and genetic variation have been found in ASD patient groups (Wen et al, 2016). Eccentric ERK activation has also been observed in peripheral lymphocytes from ASD patients (Erickson et al, 2017) and in IPSC-derived neurons from patients with 22q11.2 deletions, an intellectual disability disorder with features related to ASD (Zhao et al, 2015). In animal models, dysregulation of ERK signaling has been shown to promote the expression of ASD-like phenotypes (Faridar et al, 2014; Yufune et al, 2015).…”
Section: Potential Mechanisms Of Il-17ra Activation On Cortical Dementioning
confidence: 92%