NF-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi mathvariant="bold">κ</mml:mi></mml:math>B Signaling in the Brain of Autistic Subjects

Malik, Mazhar N.; Tauqeer, Zujaja; Sheikh, Ashfaq M.; Wen, Gen; Nagori, Amenah; Yang, Kun; Brown, W. Ted; Li, Xiaohong

doi:10.1155/2011/785265

Cited by 25 publications

(20 citation statements)

References 46 publications

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“…Also the microglia of BTBR differed from B6 in the number of MHC class II-expressing cells. These immune differences were found not to be related to changes in NF-κB signaling [107]. Similar results have recently been reported for ASD patients [108].…”

Section: Candidate Biomarkerssupporting

confidence: 80%

The BTBR T+tf/J mouse model for autism spectrum disorders–in search of biomarkers

Meyza¹,

Defensor²,

Jensen³

et al. 2013

Behavioural Brain Research

120

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Autism spectrum disorders (ASD) form a common group of neurodevelopmental disorders appearing to be under polygenic control, but also strongly influenced by multiple environmental factors. The brain mechanisms responsible for ASD are not understood and animal models paralleling related emotional and cognitive impairments may prove helpful in unraveling them. BTBR T+tf/J (BTBR) mice display behaviors consistent with the three diagnostic categories for ASD. They show impaired social interaction and communication as well as increased repetitive behaviors. This review covers much of the data available to date on BTBR behavior, neuroanatomy and physiology in search for candidate biomarkers, which could both serve as diagnostic tools and help to design effective treatments for the behavioral symptoms of ASD.

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Section: Candidate Biomarkerssupporting

confidence: 80%

The BTBR T+tf/J mouse model for autism spectrum disorders–in search of biomarkers

Meyza¹,

Defensor²,

Jensen³

et al. 2013

Behavioural Brain Research

120

View full text Add to dashboard Cite

show abstract

“…All but IgG 1 were elevated in comparison to FVB fetal brains. Despite the obvious neuroinflammatory profile, BTBR mice (and ASD patients) seem to have intact NF-κB signaling (Malik et al 2011). …”

Section: Other Physiological Aberrations Reported For the Btbr Strainmentioning

confidence: 99%

The BTBR mouse model of idiopathic autism – Current view on mechanisms

Meyza

Blanchard

2017

Neuroscience & Biobehavioral Reviews

124

109

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Autism spectrum disorder (ASD) is the most commonly diagnosed neurodevelopmental disorder, with current estimates of more than 1% of affected children across nations. The patients form a highly heterogeneous group with only the behavioral phenotype in common. The genetic heterogeneity is reflected in a plethora of animal models representing multiple mutations found in families of affected children. Despite many years of scientific effort, for the majority of cases the genetic cause remains elusive. It is therefore crucial to include well-validated models of idiopathic autism in studies searching for potential therapeutic agents. One of these models is the BTBR T+Itpr3tf/J mouse. The current review summarizes data gathered in recent research on potential molecular mechanisms responsible for the autism-like behavioral phenotype of this strain.

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“…NF- κ B has also been shown to be aberrantly expressed in the orbitofrontal cortex in patients with autism, which indicates that NF- κ B could be part of a putative molecular cascade leading to inflammation in brain regions associated with the behavioral and clinical symptoms of autism [ 60 ]. However, our laboratory results show that the expression of NF- κ B (p65) and the phosphorylation/activation of NF- κ B (p65) at Ser536 are not significantly changed in the cerebellum and cortex of both autistic subjects and BTBR mice in an autism model [ 61 ]. These findings imply that NF- κ B may be involved in the abnormal inflammatory response processes suggested in autistic brain but do not play an important part.…”

Section: Cytokines and Autismmentioning

confidence: 99%

Inflammatory Cytokines: Potential Biomarkers of Immunologic Dysfunction in Autism Spectrum Disorders

Zhong

2015

Mediators of Inflammation

Self Cite

165

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Autism is a disorder of neurobiological origin characterized by problems in communication and social skills and repetitive behavior. After more than six decades of research, the etiology of autism remains unknown, and no biomarkers have been proven to be characteristic of autism. A number of studies have shown that the cytokine levels in the blood, brain, and cerebrospinal fluid (CSF) of autistic subjects differ from that of healthy individuals; for example, a series of studies suggests that interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) are significantly elevated in different tissues in autistic subjects. However, the expression of some cytokines, such as IL-1, IL-2, transforming growth factor-β (TGF-β), and granulocyte-macrophage colony-stimulating factor (GM-CSF), is controversial, and different studies have found various results in different tissues. In this review, we focused on several types of proinflammatory and anti-inflammatory cytokines that might affect different cell signal pathways and play a role in the pathophysiological mechanism of autistic spectrum disorders.

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NF-κB Signaling in the Brain of Autistic Subjects

Cited by 25 publications

References 46 publications

The BTBR T+tf/J mouse model for autism spectrum disorders–in search of biomarkers

The BTBR T+tf/J mouse model for autism spectrum disorders–in search of biomarkers

The BTBR mouse model of idiopathic autism – Current view on mechanisms

Inflammatory Cytokines: Potential Biomarkers of Immunologic Dysfunction in Autism Spectrum Disorders

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