@article{Pichitpunpong2019,
title = {Phenotypic subgrouping and multi-omics analyses reveal reduced diazepam-binding inhibitor (DBI) protein levels in autism spectrum disorder with severe language impairment},
author = {C Pichitpunpong and S Thongkorn and S Kanlayaprasit and W Yuwattana and W Plaingam and S Sangsuthum and W M Aizat and S N Baharum and T Tencomnao and V W Hu and T Sarachana},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85063617126&doi=10.1371%2fjournal.pone.0214198&partnerID=40&md5=0a4c25481edee56984a59de94fedc414},
doi = {10.1371/journal.pone.0214198},
issn = {19326203},
year = {2019},
date = {2019-01-01},
journal = {PLoS ONE},
volume = {14},
number = {3},
publisher = {Public Library of Science},
abstract = {Background The mechanisms underlying autism spectrum disorder (ASD) remain unclear, and clinical biomarkers are not yet available for ASD. Differences in dysregulated proteins in ASD have shown little reproducibility, which is partly due to ASD heterogeneity. Recent studies have demonstrated that subgrouping ASD cases based on clinical phenotypes is useful for identifying candidate genes that are dysregulated in ASD subgroups. However, this strategy has not been employed in proteome profiling analyses to identify ASD biomarker proteins for specific subgroups. Methods We therefore conducted a cluster analysis of the Autism Diagnostic Interview-Revised (ADI-R) scores from 85 individuals with ASD to predict subgroups and subsequently identified dysregulated genes by reanalyzing the transcriptome profiles of individuals with ASD and unaffected individuals. Proteome profiling of lymphoblastoid cell lines from these individuals was performed via 2D-gel electrophoresis, and then mass spectrometry. Disrupted proteins were identified and compared to the dysregulated transcripts and reported dysregulated proteins from previous proteome studies. Biological functions were predicted using the
Ingenuity Pathway Analysis (IPA) program. Selected proteins were also analyzed by Western blotting. Results The cluster analysis of ADI-R data revealed four ASD subgroups, including ASD with severe language impairment, and transcriptome profiling identified dysregulated genes in each subgroup. Screening via proteome analysis revealed 82 altered proteins in the ASD subgroup with severe language impairment. Eighteen of these proteins were further identified by nano-LC-MS/MS. Among these proteins, fourteen were predicted by IPA to be associated with neurological functions and inflammation. Among these proteins, diazepam-binding inhibitor (DBI) protein was confirmed by Western blot analysis to be expressed at significantly decreased levels in the ASD subgroup with severe language impairment, and the DBI expression levels were correlated with the scores of several ADI-R items. Conclusions By subgrouping individuals with ASD based on clinical phenotypes, and then performing an integrated transcriptome-proteome analysis, we identified DBI as a novel candidate protein for ASD with severe language impairment. The mechanisms of this protein and its potential use as an ASD biomarker warrant further study. © 2019 Pichitpunpong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.},
note = {cited By 4},
keywords = {Article, Autism, Autism Spectrum Disorders, Binding Protein, Biological Marker, Biomarkers, Cell Line, Controlled Study, Developmental Disorders, Developmental Language Disorder, Diazepam Binding Inhibitor, Diazepam Binding Inhibitor Protein, Disease Severity, Female, Genetic Analysis, Human, Human Cell, Inflammation, Language Development Disorders, Language Disability, Liquid Chromatography-Mass Spectrometry, Lymphoblastoid Cell, Major Clinical Study, Male, Metabolism, Phenotype, Protein Analysis, Protein Expression, Protein Function, Proteome, Proteomics, Transcription Regulation, Transcriptome, Unclassified Drug, Western Blotting},
pubstate = {published},
tppubtype = {article}
}

@article{Mohamad2019343,
title = {The α5-Containing GABA A Receptors—a Brief Summary},
author = {F H Mohamad and A T C Has},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85059596842&doi=10.1007%2fs12031-018-1246-4&partnerID=40&md5=7b2ba0dc86c6c3f890f226cad8195ee5},
doi = {10.1007/s12031-018-1246-4},
issn = {08958696},
year = {2019},
date = {2019-01-01},
journal = {Journal of Molecular Neuroscience},
volume = {67},
number = {2},
pages = {343-351},
publisher = {Springer New York LLC},
abstract = {GABA A receptors are the major inhibitory neurotransmitter receptor in the human brain. The receptors are assembled from combination of protein subunits in pentameric complex which may consist of α1–6, β1–3, γ1–3, ρ1–3, δ, ε, θ, or π subunits. There are a theoretical > 150,000 possible assemblies and arrangements of GABA A subunits, although only a few combinations have been found in human with the most dominant consists of 2α1, 2β2, and 1γ2 in a counterclockwise arrangement as seen from the synaptic cleft. The receptors also possess binding sites for various unrelated substances including benzodiazepines, barbiturates, and anesthetics. The α5-containing GABA A Rs only make up ≤ 5% of the entire receptor population, but up to 25% of the receptor subtype is located in the crucial learning and memory-associated area of the brain—the hippocampus, which has ignited myriads of hypotheses and theories in regard to its role. As well as exhibiting synaptic phasic inhibition, the α5-containing receptors are also extrasynaptic and mediate tonic inhibition with continuously occurring smaller amplitude. Studies on negative-allosteric modulators for reducing this tonic inhibition have been shown to enhance learning and memory in neurological disorders such as schizophrenia, Down syndrome, and autism with a possible alternative benzodiazepine binding site. Therefore, a few α5 subunit-specific compounds have been developed to address these pharmacological needs. With its small population, the α5-containing receptors could be the key and also the answer for many untreated cognitive dysfunctions and disorders. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.},
note = {cited By 1},
keywords = {4 Aminobutyric Acid, 4 Aminobutyric Acid A Receptor, Alpha5 Containing 4 Aminobutyric Acid A Receptor, Animals, Autism, Brain, Cognitive Defect, Cognitive Dysfunction, Drug Effect, GABA Agents, GABA-A, GABAergic Receptor Affecting Agent, Genetics, Human, Metabolism, Nonhuman, Protein Subunit, Protein Subunits, Receptors, Review, Schizophrenia, Unclassified Drug},
pubstate = {published},
tppubtype = {article}
}

@article{Paudel2018145,
title = {Role of inflammation in epilepsy and neurobehavioral comorbidities: Implication for therapy},
author = {Y N Paudel and M F Shaikh and S Shah and Y Kumari and I Othman},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85053082063&doi=10.1016%2fj.ejphar.2018.08.020&partnerID=40&md5=27ff0199bae72f156425637a7ad02228},
doi = {10.1016/j.ejphar.2018.08.020},
issn = {00142999},
year = {2018},
date = {2018-01-01},
journal = {European Journal of Pharmacology},
volume = {837},
pages = {145-155},
publisher = {Elsevier B.V.},
abstract = {Epilepsy is a devastating condition affecting around 70 million people worldwide. Moreover, the quality of life of people with epilepsy (PWE) is worsened by a series of comorbidities. The neurobehavioral comorbidities discussed herein share a reciprocal and complex relationship with epilepsy, which ultimately complicates the treatment process in PWE. Understanding the mechanistic pathway by which these comorbidities are associated with epilepsy might be instrumental in developing therapeutic interventions. Inflammatory cytokine signaling in the brain regulates important brain functions including neurotransmitter metabolism, neuroendocrine function, synaptic plasticity, dopaminergic transmission, the kynurenine pathway, and affects neurogenesis as well as the neural circuitry of moods. In this review, we hypothesize that the complex relationship between epilepsy and its related comorbidities (cognitive impairment, depression, anxiety, autism, and schizophrenia) can be unraveled through the inflammatory mechanism that plays a prominent role in all these individual conditions. An ample amount of evidence is available reporting the role of inflammation in epilepsy and all individual comorbid condition but their complex relationship with epilepsy has not yet been explored through the prospective of inflammatory pathway. Our review suggests that epilepsy and its neurobehavioral comorbidities are associated with elevated levels of several key inflammatory markers. This review also sheds light on the mechanistic association between epilepsy and its neurobehavioral comorbidities. Moreover, we analyzed several anti-inflammatory therapies available for epilepsy and its neurobehavioral comorbidities. We suggest, these anti-inflammatory therapies might be a possible intervention and could be a promising strategy for preventing epileptogenesis and its related neurobehavioral comorbidities. © 2018 Elsevier B.V.},
note = {cited By 14},
keywords = {3 Dioxygenase, Acetylsalicylic Acid, Adalimumab, Anakinra, Animals, Anti-Inflammatory Agents, Anxiety, Autacoid, Autism, Autism Spectrum Disorders, Behaviour Disorder, Belnacasan, Celecoxib, Cognition, Comorbidity, Complication, Cyclooxygenase 2, Cyclooxygenase 2 Inhibitor, Cytokine, Cytokines, Depression, Dexmedetomidine, Disease Association, Dopaminergic Transmission, Electroencephalogram, Electroencephalography, Epilepsy, Epileptogenesis, Esculetin, High Mobility Group B1 Protein, Human, Ibuprofen, Icariin, IImmunoglobulin Enhancer Binding Protein, Immunology, Indoleamine 2, Inflammation, Inflammation Mediators, Infliximab, Interleukin 1beta, Interleukin 6, Minocycline, Nerve Cell Plasticity, Nervous System Development, Nervous System Inflammation, Neuroendocrine Regulation, Neurotransmitter Release, Nonhuman, Palmidrol, Paracetamol, Physiology, Priority Journal, Prostaglandin E2, Psychology, Review, SC 51089, Schizophrenia, Toll-Like Receptor 4, Transforming Growth Factor Beta, Tryptophan Hydroxylase, Tumor Necrosis Factor, Unclassified Drug},
pubstate = {published},
tppubtype = {article}
}

@article{Kho2018,
title = {The human gut microbiome - A potential controller of wellness and disease},
author = {Z Y Kho and S K Lal},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85051459505&doi=10.3389%2ffmicb.2018.01835&partnerID=40&md5=d89097ac9c0963d8ef7666aa99cff46f},
doi = {10.3389/fmicb.2018.01835},
issn = {1664302X},
year = {2018},
date = {2018-01-01},
journal = {Frontiers in Microbiology},
volume = {9},
number = {AUG},
publisher = {Frontiers Media S.A.},
abstract = {Interest toward the human microbiome, particularly gut microbiome has flourished in recent decades owing to the rapidly advancing sequence-based screening and humanized gnotobiotic model in interrogating the dynamic operations of commensal microbiota. Although this field is still at a very preliminary stage, whereby the functional properties of the complex gut microbiome remain less understood, several promising findings have been documented and exhibit great potential toward revolutionizing disease etiology and medical treatments. In this review, the interactions between gut microbiota and the host have been focused on, to provide an overview of the role of gut microbiota and their unique metabolites in conferring host protection against invading pathogen, regulation of diverse host physiological functions including metabolism, development and homeostasis of immunity and the nervous system. We elaborate on how gut microbial imbalance (dysbiosis) may lead to dysfunction of host machineries, thereby contributing to pathogenesis and/or progression toward a broad spectrum of diseases. Some of the most notable diseases namely Clostridium difficile infection (infectious disease), inflammatory bowel disease (intestinal immune-mediated disease), celiac disease (multisystemic autoimmune disorder), obesity (metabolic disease), colorectal cancer, and autism spectrum disorder (neuropsychiatric disorder) have been discussed and delineated along with recent findings. Novel therapies derived from microbiome studies such as fecal microbiota transplantation, probiotic and prebiotics to target associated diseases have been reviewed to introduce the idea of how certain disease symptoms can be ameliorated through dysbiosis correction, thus revealing a new scientific approach toward disease treatment. Toward the end of this review, several research gaps and limitations have been described along with suggested future studies to overcome the current research lacunae. Despite the ongoing debate on whether gut microbiome plays a role in the above-mentioned diseases, we have in this review, gathered evidence showing a potentially far more complex link beyond the unidirectional cause-and-effect relationship between them. © 2018 Kho and Lal.},
note = {cited By 80},
keywords = {Acetylcholine, Autism, Blood Clotting Factor 13, CD14 Antigen, Celiac Disease, Clostridium Difficile Infection, Colorectal Cancer, Cyanocobalamin, Dysbiosis, Enterotoxin, G Protein Coupled Bile Acid Receptor 1, G Protein Coupled Receptor 41, Gamma Interferon, Human, Hydrocortisone, Immunity, Immunoglobulin A, Inflammatory Bowel Disease, Interleukin 10, Interleukin 12, Interleukin 15, Interleukin 17, Interleukin 1beta, Interleukin 22, Interleukin 6, Interleukin 8, Intestine Flora, Leptin, Membrane Protein, Metabolism, Metabolite, Nervous System, Nonhuman, Obesity, Pantothenic Acid, Pathogenesis, Protein Bcl-2, Protein Expression, Protein ZO1, Review, RNA 16S, Toll-Like Receptor 4, Transcription Factor FOXP3, Tumor Necrosis Factor, Unclassified Drug, Unindexed Drug, Uvomorulin, Vasculotropin},
pubstate = {published},
tppubtype = {article}
}

@article{Gallagher201531,
title = {Ankrd11 is a chromatin regulator involved in autism that is essential for neural development},
author = {D Gallagher and A Voronova and M A Zander and G I Cancino and A Bramall and M P Krause and C Abad and M Tekin and P M Neilsen and D F Callen and S W Scherer and G M Keller and D R Kaplan and K Walz and F D Miller},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84922343890&doi=10.1016%2fj.devcel.2014.11.031&partnerID=40&md5=ad7b8bd3ead790f092e1d8a276d4f25c},
doi = {10.1016/j.devcel.2014.11.031},
issn = {15345807},
year = {2015},
date = {2015-01-01},
journal = {Developmental Cell},
volume = {32},
number = {1},
pages = {31-42},
publisher = {Cell Press},
abstract = {Ankrd11 is a potential chromatin regulator implicated in neural development and autism spectrum disorder (ASD) with no known function in the brain. Here, we show that knockdown of Ankrd11 in developing murine or human cortical neural precursors caused decreased proliferation, reduced neurogenesis, andaberrant neuronal positioning. Similar cellular phenotypes and aberrant ASD-like behaviors were observed in Yoda mice carrying a point mutation inthe Ankrd11 HDAC-binding domain. Consistent with a role for Ankrd11 in histone acetylation, Ankrd11 was associated with chromatin and colocalized with HDAC3, and expression and histone acetylation of Ankrd11 target genes were altered in Yoda neural precursors. Moreover, the Ankrd11 knockdown-mediated decrease in precursor proliferation was rescued by inhibiting histone acetyltransferase activity or expressing HDAC3. Thus, Ankrd11 is a crucial chromatin regulator that controls histone acetylation and gene expression during neural development, thereby providing a likely explanation for its association with cognitive dysfunction and ASD. © 2015 Elsevier Inc.},
note = {cited By 52},
keywords = {Acetylation, Animal Behavior, Animal Cell, Animals, Ankrd11 Protein, Ankyrin, Ankyrin Repeat Domain Containing Protein 11, Article, Autism, Autism Spectrum Disorders, Behaviour, Biological Marker, Blotting, Brain Cell Culture, Cell Culture, Cell Differentiation, Cell Proliferation, Cells, Chemistry, Chromatin, Chromatin Immunoprecipitation, Cultured, DNA Binding Protein, DNA Microarray, DNA-Binding Proteins, Enzyme Activity, Female, Gene, Gene Expression Profiling, Gene Targeting, Genetics, Histone, Histone Acetylation, Histone Acetyltransferase, Histone Deacetylase, Histone Deacetylase 3, Histone Deacetylases, Histones, Human, Human Cell, Immunoprecipitation, Messenger, Messenger RNA, Metabolism, Mice, Mouse, Murinae, Mus, Nerve Cell Differentiation, Nervous System Development, Neurogenesis, Nonhuman, Oligonucleotide Array Sequence Analysis, Pathology, Phenotype, Physiology, Point Mutation, Post-Translational, Priority Journal, Protein Expression, Protein Processing, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, RNA, Small Interfering, Small Interfering RNA, Unclassified Drug, Western, Western Blotting},
pubstate = {published},
tppubtype = {article}
}

@article{Cheah2012451,
title = {Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency},
author = {P -S Cheah and H S Ramshaw and P Q Thomas and K Toyo-Oka and X Xu and S Martin and P Coyle and M A Guthridge and F Stomski and M Van Den Buuse and A Wynshaw-Boris and A F Lopez and Q P Schwarz},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84859007028&doi=10.1038%2fmp.2011.158&partnerID=40&md5=7f507fef31a192a10b3cde7bf69b5442},
doi = {10.1038/mp.2011.158},
issn = {13594184},
year = {2012},
date = {2012-01-01},
journal = {Molecular Psychiatry},
volume = {17},
number = {4},
pages = {451-466},
abstract = {Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Here, we show that deletion of 14-3-3ζ causes neurodevelopmental anomalies similar to those seen in neuropsychiatric disorders such as schizophrenia, autism spectrum disorder and bipolar disorder. 14-3-3ζ-Deficient mice displayed striking behavioural and cognitive deficiencies including a reduced capacity to learn and remember, hyperactivity and disrupted sensorimotor gating. These deficits are accompanied by subtle developmental abnormalities of the hippocampus that are underpinned by aberrant neuronal migration. Significantly, 14-3-3ζ- deficient mice exhibited abnormal mossy fibre navigation and glutamatergic synapse formation. The molecular basis of these defects involves the schizophrenia risk factor, DISC1, which interacts isoform specifically with 14-3-3ζ. Our data provide the first evidence of a direct role for 14-3-3ζ deficiency in the aetiology of neurodevelopmental disorders and identifies 14-3-3ζ as a central risk factor in the schizophrenia protein interaction network. © 2012 Macmillan Publishers Limited All rights reserved.},
note = {cited By 58},
keywords = {14-3-3 Proteins, Animal Experiment, Animal Model, Animal Tissue, Animals, Article, Autism, Behaviour Disorder, Bipolar Disorder, Brain, Cell Movement, Cells, Cognitive Defect, Controlled Study, Cultured, Disease Models, Disrupted in Schizophrenia 1 Protein, Embryo, Female, Gene, Gene Deletion, Genetic Predisposition to Disease, Glutamic Acid, Hippocampal Mossy Fiber, Hippocampus, Human, Hyperactivity, Inbred C57BL, Isoprotein, Knockout, Learning, Male, Maze Learning, Memory, Mice, Motor Activity, Mouse, Neurogenesis, Neuronal Migration Disorder, Neurons, Neuropsychiatry, Nonhuman, Priority Journal, Protein 14-3-3, Protein 14-3-3 Zeta, Protein Deficiency, Protein Interaction, Recognition, Risk Factor, Schizophrenia, Sensory Gating, Synapse, Unclassified Drug},
pubstate = {published},
tppubtype = {article}
}