@article{Eow2020,
title = {Factors associated with autism severity among Malaysian children with Autism Spectrum Disorder},
author = {S Y Eow and W Y Gan and P Y Lim and H Awang and Z Mohd Shariff},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85081212440&doi=10.1016%2fj.ridd.2020.103632&partnerID=40&md5=a2814a66b9d649278ea7f764ed7e4125},
doi = {10.1016/j.ridd.2020.103632},
issn = {08914222},
year = {2020},
date = {2020-01-01},
journal = {Research in Developmental Disabilities},
volume = {100},
publisher = {Elsevier Inc.},
abstract = {Background: Children with Autism Spectrum Disorder (ASD) of different levels of symptom severity may exhibit a wide range of behaviours and characteristics. There is a limited nutrition-related study on children with ASD of different severity in Malaysia. Aims: This cross-sectional study aims to determine the association between sociodemographic factors, parental factors, and lifestyle factors with autism severity in children with ASD. Methods and procedures: A total of 224 children with ASD were included in this study. Their mothers completed a self-administered questionnaire on sociodemographic characteristics, autism severity, parenting style, parental feeding practices, parenting stress, child's sleep habits and eating behaviours. Outcomes and results: As high as 78.1 % of the children with ASD demonstrated a high level of autism severity. Multiple linear regression showed that father's employment status (B = 6.970, 95 % CI = 3.172, 10.768, p < 0.001) and perceived child weight (B = 3.338, 95 % CI = 1.350, 5.327},
note = {cited By 0},
keywords = {Article, Autism, Body Weight, Children, Cross-Sectional Study, Demography, Disease Association, Disease Severity, Employment, Female, Human, Lifestyle, Major Clinical Study, Malaysia, Malaysian, Male, Parents, Preschool Child, School Child, Social Status},
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}
}

@article{Nor201463,
title = {Does Bisphenol A contribute to autism spectrum disorder?},
author = {Z M Nor and S N Yusof and H F Ghazi and Z M Isa},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84939185210&partnerID=40&md5=57e7aabc3aa2ec1ab51747608ab6a9b2},
issn = {09728228},
year = {2014},
date = {2014-01-01},
journal = {Current Topics in Toxicology},
volume = {10},
pages = {63-70},
publisher = {Research Trends},
abstract = {Autism Spectrum Disorder (ASD) includes a range of conditions classified as neurodevelopmental disorders that have an onset from infancy. Multiple factors have been identified as causes for the autism spectrum disorder; however, the cascade of the disease is still not clearly defined. An increasing number of cases have been reported globally, for instance in US, UK, Canada and Australia. Environmental factors were suspected to be one of the causes. Bisphenol A (BPA) is an Endocrine Disruptor Compound (EDC) and used primarily as a monomer for the production of polycarbonate and epoxy resins, especially in feeding bottles for infants. Ongoing discussions are currently in progress on the reported low-dose effects of BPA, particularly its neurodevelopmental and behavioural effects. Many countries have banned the usage of BPA due to its harmful effects on children. This review aims at presenting an overview of the association between exposure to BPA and the neurobehavioural changes it triggers in children. Articles were obtained from the Science Direct and ProQuest search engines. The keywords used in the search were 'BPA' or 'bisphenol A' and áutism'. Fourty-seven articles were shortlisted, of which only five that fulfilled the requisite criteria were selected for review. All of them were cohort studies. Overall, an association has been established between prenatal and childhood exposure to BPA and neurobehavioural changes. The exposure during pregnancy was observed to have a greater impact on children. Earlier exposure during the prenatal period resulted in stronger associations. However, no association was found between BPA concentration of the child and neurobehavioural outcomes.},
note = {cited By 1},
keywords = {4' Isopropylidenediphenol, Article, Autism, Behaviour Change, Disease Association, Environmental Factor, First Pass Effect, Human, Population, Pregnancy, Prenatal Period},
pubstate = {published},
tppubtype = {article}
}

@article{Tan2012210,
title = {De-novo mutations and genetic variation in the SCN1A gene in Malaysian patients with generalized epilepsy with febrile seizures plus (GEFS+)},
author = {E H Tan and S A Razak and J M Abdullah and A A Mohamed Yusoff},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84870296042&doi=10.1016%2fj.eplepsyres.2012.08.004&partnerID=40&md5=25cc4eeb07db2492a7c04c6b3b3b2167},
doi = {10.1016/j.eplepsyres.2012.08.004},
issn = {09201211},
year = {2012},
date = {2012-01-01},
journal = {Epilepsy Research},
volume = {102},
number = {3},
pages = {210-215},
abstract = {Generalized epilepsy with febrile seizures plus (GEFS+) comprises a group of clinically and genetically heterogeneous epilepsy syndrome. Here, we provide the first report of clinical presentation and mutational analysis of SCN1A gene in 36 Malaysian GEFS+ patients. Mutational analysis of SCN1A gene revealed twenty seven sequence variants (missense mutation and silent polymorphism also intronic polymorphism), as well as 2 novel de-novo mutations were found in our patients at coding regions, c.5197A>G (N1733D) and c.4748A>G (H1583R). Our findings provide potential genetic insights into the pathogenesis of GEFS+ in Malaysian populations concerning the SCN1A gene mutations. © 2012 Elsevier B.V.},
note = {cited By 2},
keywords = {Alanine, Amino Acid Substitution, Arginine, Article, Asparagine, Aspartic Acid, Children, Clinical Article, Clinical Feature, Controlled Study, Disease Association, DNA Mutational Analysis, DNA Sequence, Electroencephalography, Epilepsy, Febrile, Febrile Convulsion, Female, Gene, Gene Frequency, Gene Identification, Generalized, Generalized Epilepsy, Genetic Association, Genetic Predisposition, Genetic Screening, Genetic Variability, Glycine, Histidine, Human, Infant, Malaysia, Male, Missense Mutation, Molecular Pathology, Mutation, Mutational Analysis, Mutator Gene, Nav1.1 Voltage-Gated Sodium Channel, Onset Age, Patient Assessment, Polymorphism, Preschool Child, Priority Journal, Promoter Region, School Child, Seizure, Sequence Analysis, Single Nucleotide, Single Nucleotide Polymorphism, Sodium Channel Nav1.1, Voltage Gated Sodium Channel Alpha1 Subunit Gene},
pubstate = {published},
tppubtype = {article}
}