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CNS & Neurological Disorders Drug Targets
Wednesday, November 2, 2016
Highlighted Article: Nanomaterials for Neurology: State-of-the-Art
Nanomaterials for Neurology: State-of-the-Art
Author(s):
María Fernanda Veloz-Castillo, Rachel M. West, Jessica Cordero-Arreola, Oscar Arias-Carrión and Miguel A. Méndez-Rojas Pages 1306 - 1324 ( 19 )
Abstract:
Despite the numerous challenges associated with the application of nanotechnology in neuroscience, it promises to have a significant impact on our understanding of how the nervous system works, how it fails in disease, and the development of earlier and less-invasive diagnostic procedures so we can intervene in the pre-clinical stage of neurological disease before extensive neurological damage has taken place. Ultimately, both the challenges and opportunities that nanotechnology presents stem from the fact that this technology provides a way to interact with neural cells at the molecular level. In this review we provide a neurobiological overview of key neurological disorders, describe the different types of nanomaterials in use and discuss their current and potential uses in neuroscience. We also discuss the issue of toxicity in these nanomaterials. This review presents many of the different applications that advances in nanotechnology are having in the field of neurological sciences, especially the high impact they are having in the development of new treatment modalities for neurological disorders that will induce the expected physiological response while minimizing undesirable secondary effects. In conclusion, we weigh in on what the promises and challenges are for future development in this groundbreaking field.
Keywords:
Nanomaterials, neurology, neuroscience, nanotechnology.
Affiliation:
Departamento de Ciencias Químico-Biológicas, Universidad de las Américas Puebla, Ex Hacienda Santa Catarina Mártir, San Andrés Cholula, 72820, Puebla, México.
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Tuesday, October 25, 2016
Most Cited Article: Citrus Peel Extract Attenuates Acute Cyanide Poisoning-Induced Seizures and Oxidative Stress in Rats
Citrus Peel Extract Attenuates Acute Cyanide Poisoning-Induced Seizures and Oxidative Stress in Rats
Author(s):
Ahmed E. Abdel MoneimPages 638-646 (9)
Abstract:
The primary aimed of this study was to investigate the potential protective effects of methanolic extract of citrus peel (MECP) on acute cyanide (KCN) poisoning-induced seizures and oxidative stress in rats. The intraperitoneal LD50 value of KCN (6.3 mg/Kg bwt), based on 24 hrs mortality, was significantly increased by 9, 52 or 113% by oral administration of MECP (500 mg/Kg bwt) pre-administered for 1, 2 and 3 days, respectively, in rats in a time-dependent manner. Intraperitoneal injection of the sublethal dose of KCN (3 mg/Kg bwt) into rats increased, 24 hrs later, lipid peroxidation (LPO), nitric oxide (NO), glutamate levels and acetylcholinesterase (AChE) activity in hippocampus, striatum and cerebral cortex. KCN also decreased brain glutathione (GSH) level and superoxide dismutase (SOD) and catalase (CAT) activities in these animals. Pre-treatment of rats with MECP inhibited KCN-induced increases in LPO, NO, and glutamate levels and AChE activity as well as decreases in brain GSH level and SOD and CAT activities. In addition, KCN significantly decreased norepinephrine, dopamine and serotonin levels in different brain regions which were resolved by MECP. From the present results, it can be concluded that the neuroprotective effects of MECP against KCN-induced seizures and oxidative stress may be due to the inhibition of oxidative stress overproduction and maintenance of antioxidant defense mechanisms.
Keywords:
Antioxidants, citrus peel, oxidative stress, potassium cyanide, seizures.
Affiliation:
Department of Zoology and Entomology, Faculty of Science, Helwan University, 11795 Helwan, Cairo, Egypt.
Author(s):
Ahmed E. Abdel MoneimPages 638-646 (9)
Abstract:
The primary aimed of this study was to investigate the potential protective effects of methanolic extract of citrus peel (MECP) on acute cyanide (KCN) poisoning-induced seizures and oxidative stress in rats. The intraperitoneal LD50 value of KCN (6.3 mg/Kg bwt), based on 24 hrs mortality, was significantly increased by 9, 52 or 113% by oral administration of MECP (500 mg/Kg bwt) pre-administered for 1, 2 and 3 days, respectively, in rats in a time-dependent manner. Intraperitoneal injection of the sublethal dose of KCN (3 mg/Kg bwt) into rats increased, 24 hrs later, lipid peroxidation (LPO), nitric oxide (NO), glutamate levels and acetylcholinesterase (AChE) activity in hippocampus, striatum and cerebral cortex. KCN also decreased brain glutathione (GSH) level and superoxide dismutase (SOD) and catalase (CAT) activities in these animals. Pre-treatment of rats with MECP inhibited KCN-induced increases in LPO, NO, and glutamate levels and AChE activity as well as decreases in brain GSH level and SOD and CAT activities. In addition, KCN significantly decreased norepinephrine, dopamine and serotonin levels in different brain regions which were resolved by MECP. From the present results, it can be concluded that the neuroprotective effects of MECP against KCN-induced seizures and oxidative stress may be due to the inhibition of oxidative stress overproduction and maintenance of antioxidant defense mechanisms.
Keywords:
Antioxidants, citrus peel, oxidative stress, potassium cyanide, seizures.
Affiliation:
Department of Zoology and Entomology, Faculty of Science, Helwan University, 11795 Helwan, Cairo, Egypt.
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Wednesday, October 19, 2016
Podcast on Fish Oil has Beneficial Effects on Behavior Impairment and Oxidative Stress in Rats Subjected to a Hepatic Encephalopathy Model
Podcast Fish Oil has Beneficial Effects on Behavior Impairment and Oxidative Stress in Rats Subjected to a Hepatic Encephalopathy Model
Tuesday, October 4, 2016
Podcast Ischemic Pos-Conditioning Partially Reverses Cell Cycle Reactivity Following Ischemia
Podcast Ischemic Pos-Conditioning Partially Reverses Cell Cycle Reactivity Following Ischemia
New Issue ::: CNS & Neurological Disorders – Drug Targets, 15 Issue 6
CNS & Neurological Disorders – Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular targets involved in neurological and central nervous system (CNS) disorders e.g. disease specific proteins, receptors, enzymes, genes.
CNS & Neurological Disorders – Drug Targets publishes guest edited thematic issues written by leaders in the field covering a range of current topics of CNS & neurological drug targets. The journal also accepts for publication original research articles, letters, reviews and drug clinical trial studies.
As the discovery, identification, characterization and validation of novel human drug targets for neurological and CNS drug discovery continues to grow; this journal is essential reading for all pharmaceutical scientists involved in drug discovery and development.
Articles from the journal CNS & Neurological Disorders – Drug Targets, 15 Issue 6
- Commentary: Histaminergic Drugs Could be Novel Targets for Neuroprotection in CNS Disorders
- Conference Report: 14th International Congress on Amino Acids, Peptides and Proteins, Vienna, Austria, August 3-7, 2015
- Editorial (Thematic Issue: Old Facts and New Perspectives to Face Alzheimer’s Dementia. Focus on Non Neuronal Participants to Neurodegeneration)
- Targeting New Pharmacological Approaches for Alzheimer’s Disease: Potential for Statins and Phosphodiesterase Inhibitors
- Insulin and the Future Treatment of Alzheimer’s Disease
- Adrenergic Drugs Blockers or Enhancers for Cognitive Decline ? What to Choose for Alzheimer’s Disease Patients?
- Emerging Risk Factors for Dementia: The Role of Blood Pressure Variability
- Obstructive Sleep Apnea Syndrome: An Emerging Risk Factor for Dementia
- Beyond Cholinesterase Inhibition: Anti-Inflammatory Role and Pharmacological Profile of Current Drug Therapy for Alzheimer’s Disease
- Influence of Hypertension, Alone and in Combination with Other Vascular Risk Factors on Cognition
- NLRP3 Is Involved in Ischemia/Reperfusion Injury
- Neurobiology of Bipolar Disorder: Abnormalities on Cognitive and Cortical Functioning and Biomarker Levels
- Decreased Expression of Sox-1 in Cerebellum of Rat with Generalized Seizures Induced by Kindling Model
- Preliminary Pharmacological Screening of Some Thiosemicarbazide, s-triazole, and Thiadiazole Derivatives
- Vertical and Horizontal Convergences of Targeting Pathways in Combination Therapy with Baicalin and Jasminoidin for Cerebral Ischemia
For details on the articles, please visit this link :: http://bit.ly/2aYehrv
courtesy by: Bentham Insight
Scholarly Publications by Japanese Authors in BSP Journal: CNS & Neurological Disorders – Drug Targets
CNS & Neurological Disorders – Drug TargetsImage
– Biosynthetic Pathways of Bioactive N-Acylethanolamines in Brain
Author(s): Kazuhito Tsuboi, Natsuki Ikematsu, Toru Uyama, Dale G. Deutsch, Akira Tokumura and Natsuo Ueda
Affiliation: Department of Biochemistry, Kagawa University School of Medicine, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan.
Abstract
Ethanolamides of long-chain fatty acids are a class of endogenous lipid mediators generally referred to as Nacylethanolamines (NAEs). NAEs include anti-inflammatory and analgesic palmitoylethanolamide, anorexic oleoylethanolamide, and the endocannabinoid anandamide. Since the endogenous levels of NAEs are principally regulated by enzymes responsible for their biosynthesis and degradation, these enzymes are expected as targets for the development of therapeutic agents. Thus, a better understanding of these enzymes is indispensable. The classic “N-acylationphosphodiesterase pathway” for NAE biosynthesis is composed of two steps; the formation of Nacylphosphatidylethanolamine (NAPE) by N-acyltransferase and the release of NAE from NAPE by NAPE-hydrolyzing phospholipase D (NAPE-PLD). However, recent studies, including the analysis of NAPE-PLD-deficient (NAPE-PLD-/-) mice, revealed the presence of NAPE-PLD-independent multi-step pathways to form NAEs from NAPE in animal tissues. Our recent studies using NAPE-PLD-/- mice also suggest that NAE is formed not only from NAPE, but also from Nacylated plasmalogen-type ethanolamine phospholipid (N-acyl-plasmenylethanolamine) through both NAPE-PLDdependent and -independent pathways. Here, we present recent findings on NAE biosynthetic pathways mainly occurring in the brain.
– Improving the Treatment of Schizophrenia: Role of 5-HT Receptors in Modulating Cognitive and Extrapyramidal Motor Functions
Author(s): Saki Shimizu, Yuto Mizuguchi and Yukihiro Ohno
Affiliation: Laboratory of Pharmacology, OsakaUniversity of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.
Abstract
Patients with schizophrenia exhibit various clinical symptoms including positive and negative symptoms, neurocognitive impairments and mood disturbances. Although a series of second generation antipsychotics (SGAs) (e.g., risperidone, olanzapine and quetiapine) have been developed in the past two decades, clinical reports do not necessarily show advantages over first generation antipsychotics (FGAs) in the treatment of schizophrenia, especially in their efficacy against cognitive impairment and ability to cause extrapyramidal side effects (EPS). Recently, several lines of studies have revealed therapeutic roles of 5-HT receptors in modulating cognitive impairments and extrapyramidal motor disorders. Specifically, inhibition of 5-HT1A, 5-HT3 and 5-HT6 receptors or activation of 5-HT4 receptors alleviates cognitive impairments (e.g., deficits in learning and memory). In addition, stimulation of 5-HT1A receptors or inhibition of 5-HT3and 5-HT6 receptors as well as 5-HT2A/2C receptors can ameliorate extrapyramidal motor disorders. Thus, controlling the activity of 5-HT1A, 5-HT3 or 5-HT6receptors seems to provide benefits by both alleviating cognitive impairments and reducing antipsychotic-induced EPS. This article reviews the functional roles and mechanisms of 5-HT receptors in the treatment of schizophrenia, focusing on the serotonergic modulation of cognitive and extrapyramidal motor functions, and illustrates future therapeutic strategies.
– Beyond Rodent Models of Pain: Non-Human Primate Models for Evaluating Novel Analgesic Therapeutics and Elaborating Pain Mechanisms
Author(s): Aldric T. Hama, Katsuo Toide and Hiroyuki Takamatsu
Affiliation: Hamamatsu Pharma Research, Kita-ku, 1-3-7 Shinmiyakoda, Hamamatsu 431-2103, Japan.
Abstract
Evaluation of potential analgesic therapeutics and the elaboration of the neurobiology of pain have heavily relied on pain models developed in rodents. However, a limitation of rodents is their phylogenetic distance from humans, which could in part account for the failure of some preclinical findings to translate to clinical utility. By contrast, given their genetic closeness and phenotypic similarities to humans, it is suggested that there be greater utilization of non-human primates (NHP) in preclinical pain studies. Methods to induce chronic pain-like states and quantify changes in nociception that have been developed in rodents could be adapted to the NHP. Similarly, human experimental injury-induced sensitization, which attempts to temporarily mimic the neuropathology and symptoms observed in the chronic pain state, could be adapted to the NHP. The NHP could then serve as a platform to validate human experimental models as well as proof-of-concept studies. Beyond experimentally modeled pain states, a number of naturally occurring disease states, such as osteoarthritis, are expressed by NHP, which could be utilized for both hypothesis testing and proof-of-concept studies. While NHP studies are logistically cumbersome, it is envisioned that NHP pain models will add value to current preclinical data and greatly facilitate the discovery of novel analgesic treatments.
Courtesy by Bentham Insight
Scholarly Publications by Japanese Authors in BSP Journal: CNS & Neurological Disorders – Drug Targets
CNS & Neurological Disorders – Drug TargetsImage
– Biosynthetic Pathways of Bioactive N-Acylethanolamines in Brain
Author(s): Kazuhito Tsuboi, Natsuki Ikematsu, Toru Uyama, Dale G. Deutsch, Akira Tokumura and Natsuo Ueda
Affiliation: Department of Biochemistry, Kagawa University School of Medicine, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan.
Abstract
Ethanolamides of long-chain fatty acids are a class of endogenous lipid mediators generally referred to as Nacylethanolamines (NAEs). NAEs include anti-inflammatory and analgesic palmitoylethanolamide, anorexic oleoylethanolamide, and the endocannabinoid anandamide. Since the endogenous levels of NAEs are principally regulated by enzymes responsible for their biosynthesis and degradation, these enzymes are expected as targets for the development of therapeutic agents. Thus, a better understanding of these enzymes is indispensable. The classic “N-acylationphosphodiesterase pathway” for NAE biosynthesis is composed of two steps; the formation of Nacylphosphatidylethanolamine (NAPE) by N-acyltransferase and the release of NAE from NAPE by NAPE-hydrolyzing phospholipase D (NAPE-PLD). However, recent studies, including the analysis of NAPE-PLD-deficient (NAPE-PLD-/-) mice, revealed the presence of NAPE-PLD-independent multi-step pathways to form NAEs from NAPE in animal tissues. Our recent studies using NAPE-PLD-/- mice also suggest that NAE is formed not only from NAPE, but also from Nacylated plasmalogen-type ethanolamine phospholipid (N-acyl-plasmenylethanolamine) through both NAPE-PLDdependent and -independent pathways. Here, we present recent findings on NAE biosynthetic pathways mainly occurring in the brain.
– Improving the Treatment of Schizophrenia: Role of 5-HT Receptors in Modulating Cognitive and Extrapyramidal Motor Functions
Author(s): Saki Shimizu, Yuto Mizuguchi and Yukihiro Ohno
Affiliation: Laboratory of Pharmacology, OsakaUniversity of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.
Abstract
Patients with schizophrenia exhibit various clinical symptoms including positive and negative symptoms, neurocognitive impairments and mood disturbances. Although a series of second generation antipsychotics (SGAs) (e.g., risperidone, olanzapine and quetiapine) have been developed in the past two decades, clinical reports do not necessarily show advantages over first generation antipsychotics (FGAs) in the treatment of schizophrenia, especially in their efficacy against cognitive impairment and ability to cause extrapyramidal side effects (EPS). Recently, several lines of studies have revealed therapeutic roles of 5-HT receptors in modulating cognitive impairments and extrapyramidal motor disorders. Specifically, inhibition of 5-HT1A, 5-HT3 and 5-HT6 receptors or activation of 5-HT4 receptors alleviates cognitive impairments (e.g., deficits in learning and memory). In addition, stimulation of 5-HT1A receptors or inhibition of 5-HT3and 5-HT6 receptors as well as 5-HT2A/2C receptors can ameliorate extrapyramidal motor disorders. Thus, controlling the activity of 5-HT1A, 5-HT3 or 5-HT6receptors seems to provide benefits by both alleviating cognitive impairments and reducing antipsychotic-induced EPS. This article reviews the functional roles and mechanisms of 5-HT receptors in the treatment of schizophrenia, focusing on the serotonergic modulation of cognitive and extrapyramidal motor functions, and illustrates future therapeutic strategies.
– Beyond Rodent Models of Pain: Non-Human Primate Models for Evaluating Novel Analgesic Therapeutics and Elaborating Pain Mechanisms
Author(s): Aldric T. Hama, Katsuo Toide and Hiroyuki Takamatsu
Affiliation: Hamamatsu Pharma Research, Kita-ku, 1-3-7 Shinmiyakoda, Hamamatsu 431-2103, Japan.
Abstract
Evaluation of potential analgesic therapeutics and the elaboration of the neurobiology of pain have heavily relied on pain models developed in rodents. However, a limitation of rodents is their phylogenetic distance from humans, which could in part account for the failure of some preclinical findings to translate to clinical utility. By contrast, given their genetic closeness and phenotypic similarities to humans, it is suggested that there be greater utilization of non-human primates (NHP) in preclinical pain studies. Methods to induce chronic pain-like states and quantify changes in nociception that have been developed in rodents could be adapted to the NHP. Similarly, human experimental injury-induced sensitization, which attempts to temporarily mimic the neuropathology and symptoms observed in the chronic pain state, could be adapted to the NHP. The NHP could then serve as a platform to validate human experimental models as well as proof-of-concept studies. Beyond experimentally modeled pain states, a number of naturally occurring disease states, such as osteoarthritis, are expressed by NHP, which could be utilized for both hypothesis testing and proof-of-concept studies. While NHP studies are logistically cumbersome, it is envisioned that NHP pain models will add value to current preclinical data and greatly facilitate the discovery of novel analgesic treatments.
Courtesy by Bentham Insight
Friday, August 12, 2016
Thursday, June 23, 2016
Ouabain-Induced Signaling and Cell Survival in SK-N-SH Neuroblastoma Cells Differentiated by Retinoic Acid
Author(s):
Evgeny E. Akkuratov, Jian Wu, David Sowa, Zahoor A. Shah and Lijun LiuPages 1343-1349 (7)
Abstract:
Ouabain stimulates activation of various signaling cascades such as protein kinase B (Akt) and Extracellular-signaling-regulated kinase 1/2 (ERK 1/2) in various cell lines. Retinoic acid (RA) is commonly used to induce neuroblastoma differentiation in cultures. Upon RA administration, human neuroblastoma cell line, SK-N-SH demonstrated neurite extensions, which is an indicator of neuronal cell differentiation. Here we report that ouabaininduced signaling is altered under the action of 1 μM RA in human neuroblastoma SK-N-SH cells. RA increased the expression of p110α subunit of phosphoinositide 3-kinase (PI3K), Akt and β1 subunit of Na+/K+-ATPase. Ouabain activated Akt and ERK 1/2 in differentiated SK-N-SH cells; this effect was not observed in non-differentiated SK-N-SH cells. Long-term incubation of non-differentiated SK-N-SH with 1 μM ouabain led to a decrease in the number of cells; this effect was reduced in differentiated SK-N-SH cells. Taken together, these results suggest that ouabain leads to cell death in neuroblastoma cells rather than neuronal cells due to the different response to ouabain manifested by activation of Akt and ERK 1/2.
Highlights
RA increases the expression of p110α subunit of PI3K, Akt and β1 subunit of Na+/K+-ATPase
Ouabain induces activation of Akt and ERK 1/2 in differentiated SK-N-SH cells but not in non-differentiated cells
1 µM ouabain leads to a decrease in the number of cells in non-differentiated SK-N-SH
Reduction of ouabain-induced cell death in differentiated SK-N-SH
Keywords:
Na+/K+-ATPase, neuroblastoma, ouabain, retinoic acid, phosphoinositide 3-kinase, signaling cascades.
Affiliation:
Department of Biochemistry and Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Toledo, OH, USA.
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The Effects of Testosterone Supplementation on Cognitive Functioning in Older Men.
Author(s):
Eka J. Wahjoepramono, Prita R. Asih, Vilia Aniwiyanti, Kevin Taddei, Satvinder S. Dhaliwal, Stephanie J. Fuller, Jonathan Foster, Malcolm Carruthers, Giuseppe Verdile, Hamid R Sohrabi and Ralph N. MartinsPages 337-343 (7)
Abstract:
Reduction in testosterone levels in men during aging is associated with cognitive decline and risk of dementia. Animal studies have shown benefits for testosterone supplementation in improving cognition and reducing Alzheimer’s disease pathology. In a randomized, placebo-controlled, crossover study of men with subjective memory complaint and low testosterone levels, we investigated whether testosterone treatment significantly improved performance on various measures of cognitive functioning. Forty-four men were administered a battery of neuropsychological tests to establish the baseline prior to being randomly divided into two groups. The first group (Group A) received 24 weeks of testosterone treatment (T treatment) followed by 4 weeks washout, and then 24 weeks of placebo (P); the second group (Group B) received the same treatments, in reverse order (Placebo, washout, and then T treatment). In group A (TèP), compared to baseline, there was a modest (1 point) but significant improvement in general cognitive functioning as measured by the Mini Mental State Examination (MMSE) following testosterone treatment. This improvement from baseline was sustained following the washout period and crossover to placebo treatment. Similar Mini Mental State Examination (MMSE) scores were observed when comparing testosterone treatment with placebo. In group B (PèT) a significant increase was observed from baseline following testosterone treatment and a trend towards an increase when compared to placebo treatment. Improvements in baseline depression scores (assessed by Geriatric Depression Scale) were observed following testosterone/placebo treatment in both groups, and no difference was observed when comparing testosterone with placebo treatment. Our findings indicate a modest improvement on global cognition with testosterone treatment. Larger clinical trials with a longer follow- up and with the inclusion of blood and brain imaging markers are now needed to conclusively determine the significance of testosterone treatment.
Keywords:
Testosterone, Androgen, cognition, ageing, memory, dementia, depression, Apolipoprotein E, Alzheimer’s disease.
Affiliation:
Suite 22, Hollywood Medical Centre 85 Monash Avenue, Nedlands, WA 6009, Australia
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mTOR, a Potential Target to Treat Autism Spectrum Disorder
Author(s):
Atsushi SatoPages 533-543 (11)
Abstract:
Mammalian target of rapamycin (mTOR) is a key regulator in various cellular processes, including cell growth, gene expression, and synaptic functions. Autism spectrum disorder (ASD) is frequently accompanied by monogenic disorders, such as tuberous sclerosis complex, phosphatase and tensin homolog tumor hamartoma syndrome, neurofibromatosis 1, and fragile X syndrome, in which mTOR is hyperactive. Mutations in the genes involved in the mTOR-mediated signaling pathway have been identified in some cases of syndromic ASD. Evidences indicate a pathogenic role for hyperactive mTOR-mediated signaling in ASD associated with these monogenic disorders, and mTOR inhibitors are a potential pharmacotherapy for ASD. Abnormal synaptic transmission through metabotropic glutamate receptor 5 may underlie in a part of ASD associated with hyperactive mTOR-mediated signaling. In this review, the relationship between mTOR and ASD is discussed.
Keywords:
Autophagy, fragile X syndrome, mammalian target of rapamycin, metabotropic glutamate receptor 5, neurofibromatosis, phosphatase and tensin homolog, tuberous sclerosis complex
Affiliation:
Department of Pediatrics, The University of Tokyo Hospital, Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113- 8655, Japan.
Graphical Abstract:
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The Potential of Nasal Oxytocin Administration for Remediation of Autism Spectrum Disorders
Author(s):
Yuko Okamoto, Makoto Ishitobi, Yuji Wada and Hirotaka KosakaPages 564-577 (14)
Abstract:
Administration of oxytocin has been proposed as a treatment for the core symptoms of autism spectrum disorder (ASD), including social-communicative deficit. Previous clinical trials have investigated the efficacy and safety of oxytocin intranasal single-dose and long-term administration for individuals with ASD. All studies suggest that singledose and long-term administration are well tolerated, and no severe adverse events have been reported. However, the efficacy of long-term oxytocin administration is controversial. Some studies have reported significant improvement of the core symptoms of ASD by long-term oxytocin administration, while other studies showed no such improvement. To elucidate the factors influencing the efficacy of oxytocin administration, it is necessary to examine the effects of administration schedules (e.g., dosage amount, frequency per day) and participant characteristics (e.g., age, sex, intellectual ability). In addition to doubts about the efficacy of particular methods of administration, questions remain about the mechanism of action of intranasal oxytocin on the central nervous system. Examination of changes in the neural underpinnings of social behavior and simultaneous oxytocin levels in blood or cerebrospinal fluid could prove important in elucidating the pharmacokinetics of intranasal oxytocin administration, which could be essential for establishing optimal oxytocin treatments for individuals with ASD.
Keywords:
Autism spectrum disorders, long-term administration, open-label trial, oxytocin, randomized controlled trials, single- dose, treatment.
Affiliation:
Research Center for Child Mental Development, University of Fukui, Eiheiji, Fukui 910-1193, Japan.
Graphical Abstract:
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