@artikel{Mohamad2019343,
tajuk = {The α5-Containing GABA A Receptors—a Brief Summary},
pengarang = {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&rakan kongsi = 40&md5=7b2ba0dc86c6c3f890f226cad8195ee5},
doi = {10.1007/s12031-018-1246-4},
terbitan = {08958696},
tahun = {2019},
tarikh = {2019-01-01},
jurnal = {Journal of Molecular Neuroscience},
isi padu = {67},
nombor = {2},
halaman = {343-351},
penerbit = {Springer New York LLC},
abstrak = {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, Sindrom Down, and autism with a possible alternative benzodiazepine binding site. Oleh itu, 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 + Media Perniagaan, LLC, bahagian dari Springer Nature.},
nota = {dipetik oleh 1},
kata kunci = {4 Aminobutyric Acid, 4 Aminobutyric Acid A Receptor, Alpha5 Containing 4 Aminobutyric Acid A Receptor, Haiwan, Autisme, Otak, Cognitive Defect, Cognitive Dysfunction, Drug Effect, GABA Agents, GABA-A, GABAergic Receptor Affecting Agent, Genetik, Manusia, Metabolisme, Bukan Manusia, Protein Subunit, Protein Subunits, Receptors, Kaji semula, Skizofrenia, Dadah yang tidak dikelaskan},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Khan2019186,
tajuk = {Buaya dan buaya: Jawapan doktor untuk barah?},
pengarang = {N A Khan dan M Soopramanien dan R Siddiqui},
url = {https://www.scopus.com/inward/record.uri?eid = 2-s2.0-85069313377&dua = 10.3747% 2fco.26.4855&rakan kongsi = 40&md5 = 6a266208d5fe14a1c888bb1db397d744},
doi = {10.3747/bersama.26.4855},
terbitan = {11980052},
tahun = {2019},
tarikh = {2019-01-01},
jurnal = {Onkologi Semasa},
isi padu = {26},
nombor = {3},
halaman = {186},
penerbit = {Multimed Inc.},
nota = {dipetik oleh 1},
kata kunci = {Penyakit Alergi, Buaya dan Buaya, Produk Haiwan, Haiwan, Aktiviti Antineoplastik, Ejen Antineoplastik, Artikel, Dermatitis Atopik, Autisme, Pertumbuhan Barah, Terapi Barah, Karsinogen, Organisma yang tercemar, Buaya, Kepupusan Massa Cretaceous Akhir, Faktor Persekitaran, Tekanan Alam Sekitar, Mikrobioma gastrousus, Tingkah laku Kesihatan, Logam berat, Manusia, Sistem Imun, Penyakit Usus Keradangan, Flora usus, Panjang umur, Gangguan Metabolik, Mikrobiologi, Neoplasma, Neoplasma, Pembezaan Sel Saraf, Pakar Perubatan, Skizofrenia, Analisis Survival, Penyakit Terminal},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Paudel2018145,
tajuk = {Peranan keradangan dalam epilepsi dan komorbiditi neurobehavioral: Implikasi untuk terapi},
pengarang = {Y N Paudel dan MF Shaikh dan S Shah dan Y Kumari dan I Othman},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85053082063&doi = 10.1016% 2fj.ejphar.2018.08.020&rakan kongsi = 40&md5=27ff0199bae72f156425637a7ad02228},
doi = {10.1016/j.ejphar.2018.08.020},
terbitan = {00142999},
tahun = {2018},
tarikh = {2018-01-01},
jurnal = {Jurnal Farmakologi Eropah},
isi padu = {837},
halaman = {145-155},
penerbit = {Elsevier B.V.},
abstrak = {Epilepsi adalah keadaan yang dahsyat yang menjejaskan sekeliling 70 juta orang di seluruh dunia. Lebih-lebih lagi, kualiti hidup penghidap epilepsi (PWE) diburukkan oleh beberapa siri komorbiditi. Komorbiditi neurobehavioral yang dibincangkan di sini berkongsi hubungan timbal balik dan kompleks dengan epilepsi, yang akhirnya merumitkan proses rawatan di PWE. Memahami laluan mekanistik yang mana komorbiditi ini dikaitkan dengan epilepsi mungkin memainkan peranan penting dalam membangunkan campur tangan terapeutik. Isyarat sitokin radang dalam otak mengawal fungsi otak yang penting termasuk metabolisme neurotransmitter, fungsi neuroendokrin, keplastikan sinaptik, penghantaran dopaminergik, laluan kynurenine, dan menjejaskan neurogenesis serta litar saraf mood. Dalam ulasan ini, kami membuat hipotesis bahawa hubungan kompleks antara epilepsi dan komorbiditi yang berkaitan (kecacatan kognitif, kemurungan, kegelisahan, autisme, dan skizofrenia) boleh dirungkai melalui mekanisme keradangan yang memainkan peranan penting dalam semua keadaan individu ini. Sebilangan besar bukti tersedia melaporkan peranan keradangan dalam epilepsi dan semua keadaan komorbid individu tetapi hubungan kompleks mereka dengan epilepsi masih belum diterokai melalui prospek laluan keradangan.. Kajian kami menunjukkan bahawa epilepsi dan komorbiditi neurobehavioralnya dikaitkan dengan peningkatan tahap beberapa penanda keradangan utama. Kajian ini juga memberi penerangan tentang persatuan mekanistik antara epilepsi dan komorbiditi neurobehavioralnya. Lebih-lebih lagi, kami menganalisis beberapa terapi anti-radang yang tersedia untuk epilepsi dan komorbiditi neurobehavioralnya. Kami mencadangkan, terapi anti-radang ini mungkin merupakan campur tangan yang mungkin dan boleh menjadi strategi yang menjanjikan untuk mencegah epileptogenesis dan komorbiditi neurobehavioral yang berkaitan.. © 2018 Elsevier B.V.},
nota = {dipetik oleh 14},
kata kunci = {3 Dioksigenase, Asid Acetylsalicylic, Adalimumab, Anakinra, Haiwan, Agen Anti-Radang, Keresahan, Autacoid, Autisme, Gangguan Spektrum Autisme, Gangguan Tingkah Laku, Belnacasan, Celecoxib, Kognisi, komorbiditi, Komplikasi, Cyclooxygenase 2, Cyclooxygenase 2 Perencat, Sitokin, Sitokin, Kemurungan, Dexmedetomidine, Persatuan Penyakit, Penghantaran Dopaminergik, Elektroencephalogram, Elektroensefalografi, Epilepsi, Epileptogenesis, Esculetin, Protein Kumpulan B1 Mobiliti Tinggi, Manusia, Ibuprofen, Icariin, IImmunoglobulin Enhancer Mengikat Protein, Imunologi, Indoleamine 2, Keradangan, Pengantara Inflamasi, Infliximab, Interleukin 1beta, Interleukin 6, Minocycline, Keplastikan Sel Saraf, Pembangunan Sistem Saraf, Keradangan Sistem Saraf, Peraturan Neuroendokrin, Pelepasan Neurotransmitter, Bukan Manusia, Palmidrol, Paracetamol, Fisiologi, Jurnal Keutamaan, Prostaglandin E2, Psikologi, Kaji semula, SC 51089, Skizofrenia, Reseptor Seperti Tol 4, Mengubah Faktor Pertumbuhan Beta, Tryptophan Hydroxylase, Faktor Nekrosis Tumor, Dadah yang tidak dikelaskan},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{EiThu2018865,
tajuk = {New insight in improving therapeutic efficacy of antipsychotic agents: An overview of improved in vitro and in vivo performance, efficacy upgradation and future prospects},
pengarang = {H Ei Thu and Z Hussain and A N Shuid},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85048981535&doi=10.2174%2f1389450117666161125174625&rakan kongsi = 40&md5=d32e5bc9766ff9d68dd79f082b9ca4bc},
doi = {10.2174/1389450117666161125174625},
terbitan = {13894501},
tahun = {2018},
tarikh = {2018-01-01},
jurnal = {Current Drug Targets},
isi padu = {19},
nombor = {8},
halaman = {865-876},
penerbit = {Bentham Science Publishers B.V.},
abstrak = {Psychotic disorders are recognized as severe mental disorders that rigorously affect pa-tient’s personality, critical thinking, and perceptional ability. High prevalence, global dissemination and limitations of conventional pharmacological approaches compel a significant burden to the patient, medical professionals and the healthcare system. Sehingga kini, numerous orally administered therapies are available for the management of depressive disorders, schizophrenia, kegelisahan, bipolar disorders and autism spectrum problems. Walau bagaimanapun, poor water solubility, erratic oral absorption, extensive first-pass metabolism, low oral bioavailability and short half-lives are the major factors which limit the pharmaceutical significance and therapeutic feasibility of these agents. In recent decades, nanotechnology-based delivery systems have gained remarkable attention of the researchers to mitigate the pharmaceutical issues related to the antipsychotic therapies and to optimize their oral drug delivery, therapeutic outcomes, and patient compliance. Oleh itu, the present review was aimed to summarize the available in vitro and in vivo evidences signifying the pharmaceutical importance of the advanced delivery systems in improving the aqueous solubility, transmembrane permeability, oral bioavailability and therapeutic outcome of the antipsychotic agents. © 2018 Bentham Science Publishers.},
nota = {dipetik oleh 2},
kata kunci = {Amisulpride, Amitriptyline, Haiwan, Antipsychotic Agents, Keresahan, Aripiprazole, Autisme, Bioavailability, Biological Availability, Bipolar Disorder, Buspirone, Kimia, Clonazepam, Clozapine, Kemurungan, Diazepam, Drug Delivery System, Drug Delivery Systems, Duloxetine, Half Life Time, Half-Life, Penjagaan Kesihatan, Manusia, Iloperidone, In Vitro Study, In Vivo Study, Mental Disease, Gangguan Mental, Midazolam, Nanotechnology, Neuroleptic Agent, Olanzapine, Patofisiologi, Kebolehtelapan, Physical Chemistry, Psychosis, Kaji semula, Risperidone, Skizofrenia, Solubility, Sulpiride, Hasil Rawatan, Venlafaxine, Ziprasidone},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Hakim201716,
tajuk = {Neuron-specific splicing},
pengarang = {N H A Hakim and B Y Majlis and H Suzuki and T Tsukahara},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85014435502&doi=10.5582%2fbst.2016.01169&rakan kongsi = 40&md5=8a5044dbf3b905fc2553520a048bcd59},
doi = {10.5582/bst.2016.01169},
terbitan = {18817815},
tahun = {2017},
tarikh = {2017-01-01},
jurnal = {BioScience Trends},
isi padu = {11},
nombor = {1},
halaman = {16-22},
penerbit = {International Advancement Center for Medicine and Health Research Co., Ltd.},
abstrak = {During pre-mRNA splicing events, introns are removed from the pre-mRNA, and the remaining exons are connected together to form a single continuous molecule. Alternative splicing is a common mechanism for the regulation of gene expression in eukaryotes. More than 90% of human genes are known to undergo alternative splicing. The most common type of alternative splicing is exon skipping, which is also known as cassette exon. Other known alternative splicing events include alternative 5' splice sites, alternative 3' splice sites, intron retention, and mutually exclusive exons. Alternative splicing events are controlled by regulatory proteins responsible for both positive and negative regulation. Dalam ulasan ini, we focus on neuronal splicing regulators and discuss several notable regulators in depth. Sebagai tambahan, we have also included an example of splicing regulation mediated by the RBFox protein family. Akhir kata, as previous studies have shown that a number of splicing factors are associated with neuronal diseases such as Alzheime's disease (AD) and Autism spectrum disorder (ASD), here we consider their importance in neuronal diseases wherein the underlying mechanisms have yet to be elucidated.},
nota = {dipetik oleh 0},
kata kunci = {Alternative RNA Splicing, Alternative Splicing, Haiwan, Antibody Specificity, Biological, Biological Model, Penyakit, Genetik, Manusia, Metabolisme, Models, Nerve Cell, Neurons, Organ Specificity, RNA Splicing},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Gallagher201531,
tajuk = {Ankrd11 adalah pengatur kromatin yang terlibat dalam autisme yang penting untuk perkembangan saraf},
pengarang = {D Gallagher dan A Voronova dan M A Zander dan G I Cancino dan A Bramall dan M P Krause dan C Abad dan M Tekin dan P M Neilsen dan D F Callen dan S W Scherer dan G M Keller dan D R Kaplan dan K Walz dan F D Miller},
url = {https://www.scopus.com/inward/record.uri?eid = 2-s2.0-84922343890&doi = 10.1016% 2fj.devcel.2014.11.031&rakan kongsi = 40&md5 = ad7b8bd3ead790f092e1d8a276d4f25c},
doi = {10.1016/j.devcel.2014.11.031},
terbitan = {15345807},
tahun = {2015},
tarikh = {2015-01-01},
jurnal = {Sel Perkembangan},
isi padu = {32},
nombor = {1},
halaman = {31-42},
penerbit = {Akhbar Sel},
abstrak = {Ankrd11 adalah pengatur kromatin yang berpotensi terlibat dalam perkembangan saraf dan gangguan spektrum autisme (ASD) tanpa fungsi yang diketahui di otak. Di sini, kami menunjukkan bahawa pengurangan Ankrd11 dalam mengembangkan prekursor saraf kortikal manusia atau manusia menyebabkan penurunan percambahan, neurogenesis berkurang, dan kedudukan neuron yang tidak betul. Fenotip selular yang serupa dan tingkah laku seperti ASD yang menyimpang diperhatikan pada tikus Yoda yang membawa mutasi titik dalam domain pengikat HDAC Ankrd11. Selaras dengan peranan untuk Ankrd11 dalam asetilasi histon, Ankrd11 dikaitkan dengan kromatin dan colocalized dengan HDAC3, dan ungkapan dan asetilasi histon gen sasaran Ankrd11 diubah pada pendahulu saraf Yoda. Lebih-lebih lagi, penurunan proliferasi prekursor yang dimediasi oleh Ankrd11 berjaya diselamatkan dengan menghalang aktiviti histon asetiltransferase atau menyatakan HDAC3. Oleh itu, Ankrd11 adalah pengatur kromatin penting yang mengawal asetilasi histon dan ekspresi gen semasa perkembangan saraf, sehingga memberikan penjelasan yang mungkin untuk kaitannya dengan disfungsi kognitif dan ASD. © 2015 Elsevier Inc.},
nota = {dipetik oleh 52},
kata kunci = {Asetilasi, Tingkah Laku Haiwan, Sel Haiwan, Haiwan, Protein Ankrd11, Ankyrin, Domain Ulangan Ankyrin yang Mengandungi Protein 11, Artikel, Autisme, Gangguan Spektrum Autisme, Kelakuan, Penanda Biologi, Meletup, Budaya Sel Otak, Kultur sel, Pembezaan Sel, Percambahan Sel, Sel, Kimia, Kromatin, Immunoprecipitation Chromatin, Berbudaya, Protein Mengikat DNA, Microarray DNA, Protein Pengikat DNA, Aktiviti Enzim, Perempuan, Gen, Profil Ekspresi Gen, Penyasaran Gen, Genetik, Histone, Asetilasi Histone, Histone Acetyltransferase, Histone Deacetylase, Histone Deacetylase 3, Deacetylases Histone, Histones, Manusia, Sel Manusia, Imunoprecipitasi, Utusan, Messenger RNA, Metabolisme, Tikus, Tetikus, Murinae, Mus, Pembezaan Sel Saraf, Pembangunan Sistem Saraf, Neurogenesis, Bukan Manusia, Analisis Urutan Array Oligonukleotida, Patologi, Fenotip, Fisiologi, Titik Mutasi, Pasca Terjemahan, Jurnal Keutamaan, Ekspresi Protein, Pemprosesan Protein, Tindak balas Rantai Polimerase Masa Nyata, Tindak balas Rantai Polimerase Transkrip terbalik, Reaksi Rantai Polimerase Transkripsi Berbalik, RNA, Kecil Mengganggu, RNA Mengganggu Kecil, Dadah yang tidak dikelaskan, Barat, Blotting Barat},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Karim20141213,
tajuk = {The role of viruses in neurodegenerative and neurobehavioral diseases},
pengarang = {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&rakan kongsi = 40&md5=7564c64b2fe5d0737f83e65e1fdff60a},
doi = {10.2174/187152731307141015122638},
terbitan = {18715273},
tahun = {2014},
tarikh = {2014-01-01},
jurnal = {CNS and Neurological Disorders - Drug Targets},
isi padu = {13},
nombor = {7},
halaman = {1213-1223},
penerbit = {Bentham Science Publishers B.V.},
abstrak = {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. Sehingga kini, 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.},
nota = {dipetik oleh 12},
kata kunci = {Alzheimer Disease, Amyotrophic Lateral Sclerosis, Haiwan, Artikel, Autisme, Beta Interferon, Borna Disease Virus, Cytomegalovirus, Degenerative Disease, Persatuan Penyakit, Enterovirus, Epstein Barr virus, Hepatitis Virus, Herpes Simplex Virus, HIV Associated Dementia, Manusia, Sistem Imun, Keradangan, Influenza Virus, Influenza Virus A H5N1, Mental Disease, Gangguan Mental, Multiple Sclerosis, Nerve Cell Degeneration, Neurodegenerative Diseases, Bukan Manusia, Parkinson Disease, Patofisiologi, Picornavirus, Roseolovirus, Varicella Zoster Virus, Virology, Virus Infection, Virus Pathogenesis, Virus Transmission, West Nile Flavivirus},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Cheah2012451,
tajuk = {Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency},
pengarang = {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&rakan kongsi = 40&md5=7f507fef31a192a10b3cde7bf69b5442},
doi = {10.1038/mp.2011.158},
terbitan = {13594184},
tahun = {2012},
tarikh = {2012-01-01},
jurnal = {Molecular Psychiatry},
isi padu = {17},
nombor = {4},
halaman = {451-466},
abstrak = {Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Di sini, 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.},
nota = {dipetik oleh 58},
kata kunci = {14-3-3 Proteins, Animal Experiment, Animal Model, Animal Tissue, Haiwan, Artikel, Autisme, Gangguan Tingkah Laku, Bipolar Disorder, Otak, Cell Movement, Sel, Cognitive Defect, Kajian Terkawal, Berbudaya, Disease Models, Disrupted in Schizophrenia 1 Protein, Embryo, Perempuan, Gen, Gene Deletion, Kecenderungan Genetik kepada Penyakit, Glutamic Acid, Hippocampal Mossy Fiber, Hippocampus, Manusia, Hiperaktif, Inbred C57BL, Isoprotein, Knockout, Belajar, Lelaki, Maze Learning, Memory, Tikus, Motor Activity, Tetikus, Neurogenesis, Neuronal Migration Disorder, Neurons, Neuropsychiatry, Bukan Manusia, Jurnal Keutamaan, Protein 14-3-3, Protein 14-3-3 Zeta, Protein Deficiency, Protein Interaction, Recognition, Faktor risiko, Skizofrenia, Sensory Gating, Synapse, Dadah yang tidak dikelaskan},
pubstate = {diterbitkan},
tppubtype = {artikel}
}

@artikel{Pandi-Perumal2007995,
tajuk = {Role of the melatonin system in the control of sleep: Therapeutic implications},
pengarang = {S R Pandi-Perumal and V Srinivasan and D W Spence and D P Cardinali},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-36248949004&doi=10.2165%2f00023210-200721120-00004&rakan kongsi = 40&md5=489ee976fa444beb95b26cdb77b722c2},
doi = {10.2165/00023210-200721120-00004},
terbitan = {11727047},
tahun = {2007},
tarikh = {2007-01-01},
jurnal = {CNS Drugs},
isi padu = {21},
nombor = {12},
halaman = {995-1018},
abstrak = {The circadian rhythm of pineal melatonin secretion, which is controlled by the suprachiasmatic nucleus (SCN), is reflective of mechanisms that are involved in the control of the sleep/wake cycle. Melatonin can influence sleep-promoting and sleep/wake rhythm-regulating actions through the specific activation of MT1 (melatonin 1a) and MT2 (melatonin 1b) receptors, the two major melatonin receptor subtypes found in mammals. Both receptors are highly concentrated in the SCN. In diurnal animals, exogenous melatonin induces sleep over a wide range of doses. In healthy humans, melatonin also induces sleep, although its maximum hypnotic effectiveness, as shown by studies of the timing of dose administration, is influenced by the circadian phase. In both young and elderly individuals with primary insomnia, nocturnal plasma melatonin levels tend to be lower than those in healthy controls. There are data indicating that, in affected individuals, melatonin therapy may be beneficial for ameliorating insomnia symptoms. Melatonin has been successfully used to treat insomnia in children with attention-deficit hyperactivity disorder or autism, as well as in other neurodevelopmental disorders in which sleep disturbance is commonly reported. In circadian rhythm sleep disorders, such as delayed sleep-phase syndrome, melatonin can significantly advance the phase of the sleep/wake rhythm. Begitu juga, among shift workers or individuals experiencing jet lag, melatonin is beneficial for promoting adjustment to work schedules and improving sleep quality. The hypnotic and rhythm-regulating properties of melatonin and its agonists (ramelteon, agomelatine) make them an important addition to the armamentarium of drugs for treating primary and secondary insomnia and circadian rhythm sleep disorders. © 2007 Adis Data Information BV. Hak cipta terpelihara.},
nota = {dipetik oleh 90},
kata kunci = {Absence of Side Effects, Acetylserotonin Methyltransferase, Advanced Sleep Phase Syndrome, Agomelatine, Alpha Tocopherol, Alzheimer Disease, Haiwan, Ascorbic Acid, Beta Adrenergic Receptor Blocking Agent, Biosynthesis, Circadian Rhythm, Circadian Rhythm Sleep Disorder, Clinical Trial, Confusion, Delayed Sleep Phase Syndrome, Drowsiness, Drug Dose Comparison, Drug Efficacy, Drug Half Life, Drug Mechanism, Fatigue, Fluvoxamine, Headache, Hormone Metabolism, Manusia, Hypnosis, Hypothalamus, Insomnia, Jet Lag, Macaca, Melatonin, Melatonin Receptor, Muscle Cramp, Nausea, Non-24-Hour Sleep-Wake Syndrome, Bukan Manusia, Noradrenalin, Pineal Body, Jurnal Keutamaan, Ekspresi Protein, Ramelteon, Rat Strain, Receptor Density, Receptors, REM Sleep, Retina Ganglion Cell, Kaji semula, Serotonin, Shift Worker, Sleep, Gangguan Tidur, Sleep Waking Cycle, Smith Magenis Syndrome, Suprachiasmatic Nucleus, Sustained Drug Release, Vomiting},
pubstate = {diterbitkan},
tppubtype = {artikel}
}