Alterations in neuronal cytoskeletal and astrocytic proteins content in the brain of the autistic-like mouse strain C58/J

Barón-Mendoza, Isabel; García, Otto L.; Calvo-Ochoa, Erika; Rebollar-García, Jorge Omar; Garzón-Cortés, Daniel; Haro, Reyes; González-Arenas, Aliesha

doi:10.1016/j.neulet.2018.06.004

Cited by 22 publications

(20 citation statements)

References 43 publications

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“…The phosphorylated:unphosphorylated tau ratio in the brain is in balance. One study reported alterations in the phosphorylation pattern of different tau isoforms in the hippocampus, prefrontal cortex and cerebellum of the autistic-like mice strain C58/J, suggesting that alterations in tau regulation vary between different regions of the brain [11]. The decrease in the phosphorylated:unphosphorylated tau ratio in the hippocampus in that previous study supports the idea of abnormal microtubule depolymerization [11].…”

Section: Discussionmentioning

confidence: 70%

“…One study reported alterations in the phosphorylation pattern of different tau isoforms in the hippocampus, prefrontal cortex and cerebellum of the autistic-like mice strain C58/J, suggesting that alterations in tau regulation vary between different regions of the brain [11]. The decrease in the phosphorylated:unphosphorylated tau ratio in the hippocampus in that previous study supports the idea of abnormal microtubule depolymerization [11]. Moreover, since risk gene proteins associated with ASD are found in synaptic mechanisms [9], and different tau levels have been reported in patients with ASD and controls, tau may also be an important factor in the pathogenesis of ASD.…”

Section: Discussionmentioning

confidence: 99%

“…One study showed increased expression of cathepsin D (a lysosomal protease), responsible for the formation of tau fragments predisposed to abnormal phosphorylation, in patients with ASD [10]. Moreover, alteration has been determined in the phosphorylated:unphosphorylated tau ratio, suggestive of abnormal microtubule depolymerization, in the hippocampus of autistic-like mouse strain C58/J [11]. Lower serum tau protein levels have also been determined in an autistic group compared to a control group [12].…”

Section: Introductionmentioning

confidence: 99%

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High Serum Levels of Serum 100 Beta Protein, Neuron-specific Enolase, Tau, Active Caspase-3, M30 and M65 in Children with Autism Spectrum Disorders

Ayaydın¹,

Kirmit

Çelik

et al. 2020

Clin Psychopharmacol Neurosci

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Objective: The purpose of this study was therefore to investigate whether neuronal, axonal, and glial cell markers (Neuron-specific enolase [NSE], tau, serum 100 beta protein [S100B], respectively) and apoptosis markers (active caspase 3, M30, M65) and whether these parameters can be used as diagnostic biomarkers in autism spectrum disorders (ASD). Methods: This study measured the serum S100B, NSE, tau, active caspase 3, M30, and M65 levels in 43 patients with ASD (aged 3−12 years) and in 41 age-and sex-matched healthy controls. ASD severity was rated using the Childhood Autism Rating Scale. The serum levels were determined in the biochemistry laboratory using the ELISA technique. The receiver operator characteristics curve method was employed to evaluate the accuracy of the parameters in diagnosing ASD. Results: Serum S100B, tau, NSE, active caspase-3, M30, and M65 levels were significantly higher in the patient group than in the control group (p ＜ 0.001, p = 0.002, p = 0.002, p = 0.005, p ＜ 0.001, and p = 0.004, respectively). The cutoff value of S100B was 48.085 pg/ml (sensitivity: 74.4%, specificity: 80.5%, areas under the curve: 0.879, p ＜ 0.001). Conclusion: Apoptosis increased in children with ASD, and neuronal, axonal, and glial cell injury was observed. In addition, S100B may be an important diagnostic biomarker in patients with ASD. Apoptosis, and neuronal, axonal and astrocyte pathologies may play a significant role in the pathogenesis of ASD, and further studies are now required to confirm this.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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High Serum Levels of Serum 100 Beta Protein, Neuron-specific Enolase, Tau, Active Caspase-3, M30 and M65 in Children with Autism Spectrum Disorders

Ayaydın¹,

Kirmit

Çelik

et al. 2020

Clin Psychopharmacol Neurosci

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“…Las alteraciones en la composición del citoesqueleto neuronal, en particular las anormalidades en la polimerización de los filamentos de actina y sus proteínas asociadas en el modelo de autismo en ratón cepa C58/J ( Baron-Mendoza et al, 2018), subyacen a las consecuencias funcionales en el comportamiento que resultan en síntomas y correlaciones clínicas del TEA. Una serie de estudios evidencia que la interrupción del citoesqueleto de actina a través de Rho GTPasas desreguladas contribuye al fenotipo autista (Zeidan-Chulia et al 2013;Sadybekov et al 2017).…”

Section: Citoesqueleto De Actinaunclassified

Morfología Neuronal en el Trastorno del Espectro Autista

Vásquez

Sol

2020

Int. J. Morphol.

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RESUMEN:El trastorno del espectro autista (TEA) abarca un grupo de trastornos multifactoriales del neurodesarrollo caracterizados por una comunicación e interacción social deteriorada y por comportamientos repetitivos y estereotipados. Múltiples estudios han revelado que en el TEA existen disfunciones sinápticas, en la cual la morfología y función neuronal son sustratos importantes en esta patogenia. En esta revisión comentamos los datos disponibles a nivel de anormalidades neuronales en el TEA, enfatizando la morfología de las dendritas, espinas dendríticas y citoesquelo de actina. Las dendritas y espinas dendríticas, ricas en actina, forman la parte postsináptica de la mayoría de las sinapsis excitadoras. En el TEA, los datos obtenidos apuntan a una desregulación en el crecimiento y desarrollo dendrítico, así como una alteración en la densidad de las espinas dendríticas. Lo anterior, se ve acompañado de alteraciones en la remodelación y composición del citoesqueleto neuronal. Para comprender mejor la fisiopatología del TEA, es necesario mayor información sobre cómo los cambios morfofuncionales de los actores que participan en la sinapsis impactan en los circuitos y el comportamiento.

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“…Remodeling of the actin cytoskeleton is considered as one of the critical factors associated with the autism spectrum disorders (Joensuu et al 2018). Alterations in the composition of neuronal cytoskeletal in particular abnormalities in the polymerization of actin filaments and their associated proteins have been observed in the mouse strain C58/J model of autism (Baron-Mendoza et al 2018). In the model of autism, it has been demonstrated that SHANK 3 deficient mice suffer from a loss of cortical actin filaments, in association with reduced Rho-GTPase activity together with increased activity of cofilin (Duffney et al 2015).…”

Section: Actin Cytoskeletonmentioning

confidence: 99%

Neuronal morphology alterations in autism and possible role of oxytocin

Falougy

Filová

Ostatníková

et al. 2019

Endocrine Regulations

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Current understanding of the neuroanatomical abnormalities in autism includes gross anatomical changes in several brain areas and microstructural alterations in neuronal cells as well. There are many controversies in the interpretation of the imaging data, evaluation of volume and size of particular brain areas, and their functional translation into a broad autism phenotype. Critical questions of neuronal pathology in autism include the concept of the reversible plasticity of morphological changes, volume alterations of brain areas, and both short- and long-term consequences of adverse events present during the brain development. At the cellular level, remodeling of the actin cytoskeleton is considered as one of the critical factors associated with the autism spectrum disorders. Alterations in the composition of the neuronal cytoskeleton, in particular abnormalities in the polymerization of actin filaments and their associated proteins underlie the functional consequences in behavior resulting in symptoms and clinical correlates of autism spectrum disorder. In the present review, a special attention is devoted to the role of oxytocin in experimental models of neurodevelopmental disorders manifesting alterations in neuronal morphology.

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Alterations in neuronal cytoskeletal and astrocytic proteins content in the brain of the autistic-like mouse strain C58/J

Cited by 22 publications

References 43 publications

High Serum Levels of Serum 100 Beta Protein, Neuron-specific Enolase, Tau, Active Caspase-3, M30 and M65 in Children with Autism Spectrum Disorders

High Serum Levels of Serum 100 Beta Protein, Neuron-specific Enolase, Tau, Active Caspase-3, M30 and M65 in Children with Autism Spectrum Disorders

Morfología Neuronal en el Trastorno del Espectro Autista

Neuronal morphology alterations in autism and possible role of oxytocin

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