@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{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{Karim20141213,
title = {The role of viruses in neurodegenerative and neurobehavioral diseases},
author = {S Karim and Z Mirza and M A Kamal and A M Abuzenadah and E I Azhar and M H Al-Qahtani and G A Damanhouri and F Ahmad and S H Gan and S S Sohrab},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84911396470&doi=10.2174%2f187152731307141015122638&partnerID=40&md5=7564c64b2fe5d0737f83e65e1fdff60a},
doi = {10.2174/187152731307141015122638},
issn = {18715273},
year = {2014},
date = {2014-01-01},
journal = {CNS and Neurological Disorders - Drug Targets},
volume = {13},
number = {7},
pages = {1213-1223},
publisher = {Bentham Science Publishers B.V.},
abstract = {Neurodegenerative and neurobehavioral diseases may be caused by chronic and neuropathic viral infections and may result in a loss of neurons and axons in the central nervous system that increases with age. To date, there is evidence of systemic viral infections that occur with some neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, autism spectrum disorders, and HIV-associated neurocognitive disorders. With increasing lifespan, the incidence of neurodegenerative diseases increases consistently. Neurodegenerative diseases affect approximately 37 million people worldwide and are an important cause of mortality. In addition to established non-viral-induced reasons for neurodegenerative diseases, neuropathic infections and viruses associated with neurodegenerative diseases have been proposed. Neuronal degeneration can be either directly or indirectly affected by viral infection. Viruses that attack the human immune system can also affect the nervous system and interfere with classical pathways of neurodegenerative diseases. Viruses can enter the central nervous system, but the exact mechanism cannot be understood well. Various studies have supported viral- and non-viral-mediated neurodegeneration at the cellular, molecular, genomic and proteomic levels. The main focus of this review is to illustrate the association between viral infections and both neurodegenerative and neurobehavioral diseases, so that the possible mechanism and pathway of neurodegenerative diseases can be better explained. This information will strengthen new concepts and ideas for neurodegenerative and neurobehavioral disease treatment. © 2014 Bentham Science Publishers.},
note = {cited By 12},
keywords = {Alzheimer Disease, Amyotrophic Lateral Sclerosis, Animals, Article, Autism, Beta Interferon, Borna Disease Virus, Cytomegalovirus, Degenerative Disease, Disease Association, Enterovirus, Epstein Barr virus, Hepatitis Virus, Herpes Simplex Virus, HIV Associated Dementia, Human, Immune System, Inflammation, Influenza Virus, Influenza Virus A H5N1, Mental Disease, Mental Disorders, Multiple Sclerosis, Nerve Cell Degeneration, Neurodegenerative Diseases, Nonhuman, Parkinson Disease, Pathophysiology, Picornavirus, Roseolovirus, Varicella Zoster Virus, Virology, Virus Infection, Virus Pathogenesis, Virus Transmission, West Nile Flavivirus},
pubstate = {published},
tppubtype = {article}
}