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Terdapat sebilangan besar penyelidikan berkaitan autisme yang boleh dijumpai di Malaysia yang umumnya menumpukan pada ASD, gangguan pembelajaran, alat bantu komunikasi, terapi dan banyak lagi. Senarai penerbitan disediakan di bawah:
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2019 |
Prabhakar, S; Cheah, P S; Zhang, X; Zinter, M; Gianatasio, M; Hudry, E; Bronson, R T; Kwiatkowski, D J; Stemmer-Rachamimov, A; Maguire, C A; Sena-Esteves, M; Tannous, B A; Breakefield, X O Long-Term Therapeutic Efficacy of Intravenous AAV-Mediated Hamartin Replacement in Mouse Model of Tuberous Sclerosis Type 1 Artikel Jurnal Molecular Therapy - Methods and Clinical Development, 15 , hlm. 18-26, 2019, ISSN: 23290501, (dipetik oleh 2). Abstrak | Pautan | BibTeX | Tag: Adeno Associated Virus, Adeno Associated Virus Vector, Animal Experiment, Animal Model, Artikel, Beta Actin, Blood Brain Barrier, Berat badan, Body Weight Gain, Brain Nerve Cell, Brain Ventricle, Percambahan Sel, Complementary DNA, Kajian Terkawal, Cre Recombinase, Drug Efficacy, Perempuan, Gen, Gene Replacement Therapy, Hamartin, HEK293 Cell Line, Hydrocephalus, Immunohistochemistry, Inverted Terminal Repeat, Long Term Care, Lelaki, Motor Activity, Motor Performance, Tetikus, Bukan Manusia, Jurnal Keutamaan, Promoter Region, Fungsi Protein, Protein Phosphorylation, Quantitative Analysis, Subventricular Zone, Survival Time, Tuberous Sclerosis, Tuberous Sclerosis Type 1, Vascularization, Viral Gene Delivery System @artikel{Prabhakar201918, tajuk = {Long-Term Therapeutic Efficacy of Intravenous AAV-Mediated Hamartin Replacement in Mouse Model of Tuberous Sclerosis Type 1}, pengarang = {S Prabhakar and P S Cheah and X Zhang and M Zinter and M Gianatasio and E Hudry and R T Bronson and D J Kwiatkowski and A Stemmer-Rachamimov and C A Maguire and M Sena-Esteves and B A Tannous and X O Breakefield}, url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85070908794&doi=10.1016%2fj.omtm.2019.08.003&rakan kongsi = 40&md5=b169187dde0d3b05f8a9d5295a4ad8c4}, doi = {10.1016/j.omtm.2019.08.003}, terbitan = {23290501}, tahun = {2019}, tarikh = {2019-01-01}, jurnal = {Molecular Therapy - Methods and Clinical Development}, isi padu = {15}, halaman = {18-26}, penerbit = {Akhbar Sel}, abstrak = {Tuberous sclerosis complex (TSC) is a tumor suppressor syndrome caused by mutations in TSC1 or TSC2, encoding hamartin and tuberin, masing-masing. These proteins act as a complex that inhibits mammalian target of rapamycin (mTOR)-mediated cell growth and proliferation. Loss of either protein leads to overgrowth in many organs, including subependymal nodules, subependymal giant cell astrocytomas, and cortical tubers in the human brain. Neurological manifestations in TSC include intellectual disability, autisme, hydrocephalus, and epilepsy. In a stochastic mouse model of TSC1 brain lesions, complete loss of Tsc1 is achieved in homozygous Tsc1-floxed mice in a subpopulation of neural cells in the brain by intracerebroventricular (i.c.v.) injection at birth of an adeno-associated virus (AAV) vector encoding Cre recombinase. This results in median survival of 38 days and brain pathology, including subependymal lesions and enlargement of neuronal cells. Remarkably, when these mice were injected intravenously on day 21 with an AAV9 vector encoding hamartin, most survived at least up to 429 days in apparently healthy condition with marked reduction in brain pathology. Oleh itu, a single intravenous administration of an AAV vector encoding hamartin restored protein function in enough cells in the brain to extend lifespan in this TSC1 mouse model. © 2019}, nota = {dipetik oleh 2}, kata kunci = {Adeno Associated Virus, Adeno Associated Virus Vector, Animal Experiment, Animal Model, Artikel, Beta Actin, Blood Brain Barrier, Berat badan, Body Weight Gain, Brain Nerve Cell, Brain Ventricle, Percambahan Sel, Complementary DNA, Kajian Terkawal, Cre Recombinase, Drug Efficacy, Perempuan, Gen, Gene Replacement Therapy, Hamartin, HEK293 Cell Line, Hydrocephalus, Immunohistochemistry, Inverted Terminal Repeat, Long Term Care, Lelaki, Motor Activity, Motor Performance, Tetikus, Bukan Manusia, Jurnal Keutamaan, Promoter Region, Fungsi Protein, Protein Phosphorylation, Quantitative Analysis, Subventricular Zone, Survival Time, Tuberous Sclerosis, Tuberous Sclerosis Type 1, Vascularization, Viral Gene Delivery System}, pubstate = {diterbitkan}, tppubtype = {artikel} } Tuberous sclerosis complex (TSC) is a tumor suppressor syndrome caused by mutations in TSC1 or TSC2, encoding hamartin and tuberin, masing-masing. These proteins act as a complex that inhibits mammalian target of rapamycin (mTOR)-mediated cell growth and proliferation. Loss of either protein leads to overgrowth in many organs, including subependymal nodules, subependymal giant cell astrocytomas, and cortical tubers in the human brain. Neurological manifestations in TSC include intellectual disability, autisme, hydrocephalus, and epilepsy. In a stochastic mouse model of TSC1 brain lesions, complete loss of Tsc1 is achieved in homozygous Tsc1-floxed mice in a subpopulation of neural cells in the brain by intracerebroventricular (i.c.v.) injection at birth of an adeno-associated virus (AAV) vector encoding Cre recombinase. This results in median survival of 38 days and brain pathology, including subependymal lesions and enlargement of neuronal cells. Remarkably, when these mice were injected intravenously on day 21 with an AAV9 vector encoding hamartin, most survived at least up to 429 days in apparently healthy condition with marked reduction in brain pathology. Oleh itu, a single intravenous administration of an AAV vector encoding hamartin restored protein function in enough cells in the brain to extend lifespan in this TSC1 mouse model. © 2019 |
Mohamad, F H; Telah, A T C The α5-Containing GABA A Receptors—a Brief Summary Artikel Jurnal Journal of Molecular Neuroscience, 67 (2), hlm. 343-351, 2019, ISSN: 08958696, (dipetik oleh 1). Abstrak | Pautan | BibTeX | Tag: 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 @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} } 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. |
2018 |
Paudel, Y N; Syeikh, M F; Shah, S; Kumari, Y; Othman, Saya Peranan keradangan dalam epilepsi dan komorbiditi neurobehavioral: Implikasi untuk terapi Artikel Jurnal Jurnal Farmakologi Eropah, 837 , hlm. 145-155, 2018, ISSN: 00142999, (dipetik oleh 14). Abstrak | Pautan | BibTeX | Tag: 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 @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} } 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. |
Gudang, Dengan Y; Lal, S K The human gut microbiome - A potential controller of wellness and disease Artikel Jurnal Frontiers in Microbiology, 9 (AUG), 2018, ISSN: 1664302X, (dipetik oleh 80). Abstrak | Pautan | BibTeX | Tag: Acetylcholine, Autisme, 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, Manusia, Hydrocortisone, Immunity, Immunoglobulin A, Penyakit Usus Keradangan, Interleukin 10, Interleukin 12, Interleukin 15, Interleukin 17, Interleukin 1beta, Interleukin 22, Interleukin 6, Interleukin 8, Flora usus, Leptin, Protein Membran, Metabolisme, Metabolite, Nervous System, Bukan Manusia, Obesiti, Pantothenic Acid, Pathogenesis, Protein Bcl-2, Ekspresi Protein, Protein ZO1, Kaji semula, RNA 16S, Reseptor Seperti Tol 4, Transcription Factor FOXP3, Faktor Nekrosis Tumor, Dadah yang tidak dikelaskan, Unindexed Drug, Uvomorulin, Vasculotropin @artikel{Kho2018, tajuk = {The human gut microbiome - A potential controller of wellness and disease}, pengarang = {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&rakan kongsi = 40&md5=d89097ac9c0963d8ef7666aa99cff46f}, doi = {10.3389/fmicb.2018.01835}, terbitan = {1664302X}, tahun = {2018}, tarikh = {2018-01-01}, jurnal = {Frontiers in Microbiology}, isi padu = {9}, nombor = {AUG}, penerbit = {Frontiers Media S.A.}, abstrak = {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. Dalam ulasan ini, 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.}, nota = {dipetik oleh 80}, kata kunci = {Acetylcholine, Autisme, 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, Manusia, Hydrocortisone, Immunity, Immunoglobulin A, Penyakit Usus Keradangan, Interleukin 10, Interleukin 12, Interleukin 15, Interleukin 17, Interleukin 1beta, Interleukin 22, Interleukin 6, Interleukin 8, Flora usus, Leptin, Protein Membran, Metabolisme, Metabolite, Nervous System, Bukan Manusia, Obesiti, Pantothenic Acid, Pathogenesis, Protein Bcl-2, Ekspresi Protein, Protein ZO1, Kaji semula, RNA 16S, Reseptor Seperti Tol 4, Transcription Factor FOXP3, Faktor Nekrosis Tumor, Dadah yang tidak dikelaskan, Unindexed Drug, Uvomorulin, Vasculotropin}, pubstate = {diterbitkan}, tppubtype = {artikel} } 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. Dalam ulasan ini, 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. |
2015 |
Gallagher, D; Voronova, A; Zander, M A; Cancun, G I; Bramall, A; Krause, M P; Abad, C; Tekin, M; Neilsen, P M; Callen, D F; Scherer, S W; Pembunuh, G M; Kaplan, D R; Walz, K; Miller, F D Ankrd11 adalah pengatur kromatin yang terlibat dalam autisme yang penting untuk perkembangan saraf Artikel Jurnal Sel Perkembangan, 32 (1), hlm. 31-42, 2015, ISSN: 15345807, (dipetik oleh 52). Abstrak | Pautan | BibTeX | Tag: 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 @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} } 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.. |
2014 |
Karim, S; Mirza, DENGAN; Kamal, M A; Abuzenadah, Seorang M; Azhar, E Saya; Al-Qahtani, M H; Damanhouri, G A; Ahmad, F; Gan, S H; Sohrab, S S The role of viruses in neurodegenerative and neurobehavioral diseases Artikel Jurnal CNS and Neurological Disorders - Drug Targets, 13 (7), hlm. 1213-1223, 2014, ISSN: 18715273, (dipetik oleh 12). Abstrak | Pautan | BibTeX | Tag: 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 @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} } 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. |
2012 |
Cheah, P -S; Ramshaw, H S; Thomas, P; Toyo-Oka, K; Syiling, X; Martin, S; Coyle, P; Guthridge, M A; Stomski, F; Tetapi, Van Den M; Wynshaw-Boris, A; Lopez, A F; Schwarz, Q Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency Artikel Jurnal Molecular Psychiatry, 17 (4), hlm. 451-466, 2012, ISSN: 13594184, (dipetik oleh 58). Abstrak | Pautan | BibTeX | Tag: 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 @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} } 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. |
2007 |
Pandi-Perumal, S R; Srinivasan, V; Spence, D W; Kardinal, D P Role of the melatonin system in the control of sleep: Therapeutic implications Artikel Jurnal CNS Drugs, 21 (12), hlm. 995-1018, 2007, ISSN: 11727047, (dipetik oleh 90). Abstrak | Pautan | BibTeX | Tag: 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 @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} } 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. |