@article{Masiran2018b,
title = {Autism and trichotillomania in an adolescent boy},
author = {R Masiran},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85053164449&doi=10.1136%2fbcr-2018-226270&partnerID=40&md5=7eed3f6af717df527dce73838feab571},
doi = {10.1136/bcr-2018-226270},
issn = {1757790X},
year = {2018},
date = {2018-01-01},
journal = {BMJ Case Reports},
volume = {2018},
publisher = {BMJ Publishing Group},
abstract = {An adolescent with autism spectrum disorder and improperly treated attention deficit hyperactivity disorder presented with recurrent hair pulling. Treatment with selective serotonin reuptake inhibitor and stimulant improved these conditions. © © BMJ Publishing Group Limited 2018.},
note = {cited By 0},
keywords = {Adolescent, Alopecia, Anxiety, Article, Attention Deficit Disorder, Attention Deficit Hyperactivity Disorder, Autism, Autism Spectrum Disorders, Behaviour Disorder, Body Mass, Case Report, Central Nervous System Stimulants, Child Behaviour Checklist, Clinical Article, Comorbidity, Complication, Diagnosis, Differential, Differential Diagnosis, Drug Dose Titration, Drug Tolerance, DSM-5, Echolalia, Fluvoxamine, Follow Up, Human, Hyperactivity, Intellectual Impairment, Male, Methylphenidate, Obesity, Occupational Therapy, Perceptual Reasoning Index, Priority Journal, Processing Speed Index, Psychiatric Status Rating Scales, Psychological Rating Scale, Rating Scale, Restlessness, Reward, Serotonin Uptake Inhibitor, Serotonin Uptake Inhibitors, Special Education, Speech Delay, Speech Disorder, Speech Therapy, Trichotillomania, Verbal Comprehension Index, Wechsler Intelligence Scale, Working Memory Index},
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{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}
}