Pub Date : 2020-07-21DOI: 10.31117/neuroscirn.v3i3.51
P. Cheah, K. Ling, Eric Tatt Wei Ho
Neuroscience has emerged as a richly transdisciplinary field, poised to leverage potential synergies with information technology. To investigate the complex nervous system in its normal function and the disease state, researchers in the field are increasingly reliant on generating, sharing and analyzing diverse data from multiple experimental paradigms at multiple spatial and temporal scales. There is growing recognition that brain function must be investigated from a systems perspective. This requires an integrated analysis of genomic, proteomic, anatomical, functional, topological and behavioural information to arrive at accurate scientific conclusions. The integrative neuroinformatics approaches for exploring complex structure-function relationships in the nervous system have been extensively reviewed. To support neuroscience research, the neuroscientific community also generates and maintains web-accessible databases of experimental and computational data and innovative software tools. Neuroinformatics is an emerging sub-field of neuroscience which focuses on addressing the unique technological and computational challenges to integrate and analyze the increasingly high-volume, multi-dimensional, and fine-grain data generated from neuroscience experiments. The most visible contributions from neuroinformatics include the myriad reference atlases of brain anatomy (human and other mammals such as rodents, primates and pig), gene and protein sequences and the bioinformatics software tools for alignment, matching and identification. Other neuroinformatics initiatives include the various open-source preprocessing and processing software and workflows for data analysis as well as the specifications for data format and software interoperability that allow seamless exchange of data between labs, software tools and modalities.
{"title":"From online resources to collaborative global neuroscience research: where are we heading?","authors":"P. Cheah, K. Ling, Eric Tatt Wei Ho","doi":"10.31117/neuroscirn.v3i3.51","DOIUrl":"https://doi.org/10.31117/neuroscirn.v3i3.51","url":null,"abstract":"Neuroscience has emerged as a richly transdisciplinary field, poised to leverage potential synergies with information technology. To investigate the complex nervous system in its normal function and the disease state, researchers in the field are increasingly reliant on generating, sharing and analyzing diverse data from multiple experimental paradigms at multiple spatial and temporal scales. There is growing recognition that brain function must be investigated from a systems perspective. This requires an integrated analysis of genomic, proteomic, anatomical, functional, topological and behavioural information to arrive at accurate scientific conclusions. The integrative neuroinformatics approaches for exploring complex structure-function relationships in the nervous system have been extensively reviewed. To support neuroscience research, the neuroscientific community also generates and maintains web-accessible databases of experimental and computational data and innovative software tools. Neuroinformatics is an emerging sub-field of neuroscience which focuses on addressing the unique technological and computational challenges to integrate and analyze the increasingly high-volume, multi-dimensional, and fine-grain data generated from neuroscience experiments. The most visible contributions from neuroinformatics include the myriad reference atlases of brain anatomy (human and other mammals such as rodents, primates and pig), gene and protein sequences and the bioinformatics software tools for alignment, matching and identification. Other neuroinformatics initiatives include the various open-source preprocessing and processing software and workflows for data analysis as well as the specifications for data format and software interoperability that allow seamless exchange of data between labs, software tools and modalities.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42570240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-05-30DOI: 10.31117/neuroscirn.v3i2.48
Kavinash Loganathan, Eric Tatt Wei Ho
In Malaysia, abstinence-centric programs failed to reduce drug use and stem the spread of HIV. The Malaysian government shifted its focus to implement harm reduction strategies with methadone maintenance therapy (MMT), in particular proving to be effective in improving the overall health and well-being of people who inject drugs (PWIDs). Despite this success, MMT retention rates remain low, as methadone is only able to stall drug consumption, but not stop it completely. Neuroimaging research revealed that PWIDs enrolled in MMT still display addictive behavior, including drug cue sensitivity, craving, and withdrawal, despite treatment adherence. Brain activity amongst treated PWIDs continues to bear similarities to untreated individuals, as they struggle with cognitive impairments and poor self-control. Findings from the emerging field of network neuroscience could provide fresh insight into the mechanics of addiction, especially the impact of substance abuse on brain-wide cognitive networks. Concurrently, the development of non-intrusive cognitive interventions, such as neurofeedback and transcranial magnetic stimulation, shows promise to reprogram a person's patterns of brain activity, including those regulated by large-scale networks, to a state resembling normalcy. We highlight the importance of relapse in the life-long rehabilitation of substance abuse. The lack of treatment options to handle relapse after successful harm-reduction policies is due to the absence of a conceptual framework to reason about interventions. We review recent research in the new field of network neuroscience, which suggests that altered brain activity due to drug addiction underlies the propensity for relapse and that this dysfunction is not addressed in drug rehabilitation programs. We hypothesize that non-invasive, non-pharmacological cognitive interventions based on network neuroscience to correct brain activity dysfunction associated with addiction are potential therapies to treat drug addiction relapse. In complement with medicine-substitution-based therapies, we hope this approach will finally break the cycle of addiction.
{"title":"Neurocognitive interventions based on network neuroscience may break the cycle of drug addiction relapse","authors":"Kavinash Loganathan, Eric Tatt Wei Ho","doi":"10.31117/neuroscirn.v3i2.48","DOIUrl":"https://doi.org/10.31117/neuroscirn.v3i2.48","url":null,"abstract":"In Malaysia, abstinence-centric programs failed to reduce drug use and stem the spread of HIV. The Malaysian government shifted its focus to implement harm reduction strategies with methadone maintenance therapy (MMT), in particular proving to be effective in improving the overall health and well-being of people who inject drugs (PWIDs). Despite this success, MMT retention rates remain low, as methadone is only able to stall drug consumption, but not stop it completely. Neuroimaging research revealed that PWIDs enrolled in MMT still display addictive behavior, including drug cue sensitivity, craving, and withdrawal, despite treatment adherence. Brain activity amongst treated PWIDs continues to bear similarities to untreated individuals, as they struggle with cognitive impairments and poor self-control. Findings from the emerging field of network neuroscience could provide fresh insight into the mechanics of addiction, especially the impact of substance abuse on brain-wide cognitive networks. Concurrently, the development of non-intrusive cognitive interventions, such as neurofeedback and transcranial magnetic stimulation, shows promise to reprogram a person's patterns of brain activity, including those regulated by large-scale networks, to a state resembling normalcy. We highlight the importance of relapse in the life-long rehabilitation of substance abuse. The lack of treatment options to handle relapse after successful harm-reduction policies is due to the absence of a conceptual framework to reason about interventions. We review recent research in the new field of network neuroscience, which suggests that altered brain activity due to drug addiction underlies the propensity for relapse and that this dysfunction is not addressed in drug rehabilitation programs. We hypothesize that non-invasive, non-pharmacological cognitive interventions based on network neuroscience to correct brain activity dysfunction associated with addiction are potential therapies to treat drug addiction relapse. In complement with medicine-substitution-based therapies, we hope this approach will finally break the cycle of addiction.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42449655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-05-29DOI: 10.31117/neuroscirn.v3i2.49
D. Abdullahi, A. A. Annuar, J. Sanusi
Experimental studies on spinal cord regeneration are focusing on the windows of opportunity to improve spinal cord microenvironment via spinal-centric repair pathways. One pathway of particular interest is the Wnt/β-catenin signalling pathway which plays a vital role in axonal guidance, synaptic assembly and function, neuronal survival and connectivity after spinal cord trauma to induce repair. Upregulation of β-catenin expression is often taken as evidence of regeneration mechanisms through the Wnt/ β-catenin pathway. However, these studies may not have optimised the staining protocol for β-catenin to enable accurate detection of the protein. Given possible issues with the background or endogenous tissue autofluorescence, there is a need to optimise the protocol further to allow better visualisation of β-catenin. So far, there are no studies which report optimising spinal cord tissues for β-catenin to reduce autofluorescence, and as β-catenin is widely used in spinal cord injury (SCI) and other spinal cord tissue studies, thus it is an important issue to address. To achieve reliable detection and localisation of β-catenin, we utilised sequential quenching techniques using 1% NaBH4 and 1mM CuSO4 in 50mM ammonium acetate buffer to reduce both background and fixative-induced autofluorescence. Our results showed that sequential autofluorescence quenching is crucial in β-catenin detection, and this improved technique indicates that β-catenin is localised in the spinal cord white matter regions. Objective approach for the β-catenin localisation is highly significant as it unravelled an objective identification and illuminate the pattern of distribution of β-catenin for researcher focusing on spinal cord repair studies via the Wnt/β-catenin pathway following SCI.
{"title":"Improved β-catenin detection in spinal cord tissue sections: autofluorescence quenching","authors":"D. Abdullahi, A. A. Annuar, J. Sanusi","doi":"10.31117/neuroscirn.v3i2.49","DOIUrl":"https://doi.org/10.31117/neuroscirn.v3i2.49","url":null,"abstract":"Experimental studies on spinal cord regeneration are focusing on the windows of opportunity to improve spinal cord microenvironment via spinal-centric repair pathways. One pathway of particular interest is the Wnt/β-catenin signalling pathway which plays a vital role in axonal guidance, synaptic assembly and function, neuronal survival and connectivity after spinal cord trauma to induce repair. Upregulation of β-catenin expression is often taken as evidence of regeneration mechanisms through the Wnt/ β-catenin pathway. However, these studies may not have optimised the staining protocol for β-catenin to enable accurate detection of the protein. Given possible issues with the background or endogenous tissue autofluorescence, there is a need to optimise the protocol further to allow better visualisation of β-catenin. So far, there are no studies which report optimising spinal cord tissues for β-catenin to reduce autofluorescence, and as β-catenin is widely used in spinal cord injury (SCI) and other spinal cord tissue studies, thus it is an important issue to address. To achieve reliable detection and localisation of β-catenin, we utilised sequential quenching techniques using 1% NaBH4 and 1mM CuSO4 in 50mM ammonium acetate buffer to reduce both background and fixative-induced autofluorescence. Our results showed that sequential autofluorescence quenching is crucial in β-catenin detection, and this improved technique indicates that β-catenin is localised in the spinal cord white matter regions. Objective approach for the β-catenin localisation is highly significant as it unravelled an objective identification and illuminate the pattern of distribution of β-catenin for researcher focusing on spinal cord repair studies via the Wnt/β-catenin pathway following SCI.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44566354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-04-04DOI: 10.31117/neuroscirn.v3i2.46
M. Shaikh, F. A. Shaikh
The genetic epidemiology suggests that coronavirus disease 2019 (COVID-19) is most likely transmitted to the human population in November or December 2019, originating from Wuhan and spread entirely by human-to-human transmission. The period of the Chinese New Year holidays is thought to be one of the key periods where a substantial transmission took place within Wuhan. Moreover, the movement of people from Wuhan resulted in massive spread nationally and internationally when people traveled during the holidays.
{"title":"COVID-19 and mental health: Our reactions to its actions","authors":"M. Shaikh, F. A. Shaikh","doi":"10.31117/neuroscirn.v3i2.46","DOIUrl":"https://doi.org/10.31117/neuroscirn.v3i2.46","url":null,"abstract":"The genetic epidemiology suggests that coronavirus disease 2019 (COVID-19) is most likely transmitted to the human population in November or December 2019, originating from Wuhan and spread entirely by human-to-human transmission. The period of the Chinese New Year holidays is thought to be one of the key periods where a substantial transmission took place within Wuhan. Moreover, the movement of people from Wuhan resulted in massive spread nationally and internationally when people traveled during the holidays.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43828736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-30DOI: 10.31117/NEUROSCIRN.V3I1.40
R. Pérez-Elvira, Ana Jiménez Gómez
Fibromyalgia is a chronic and incapacitating condition that produces, as main symptoms, pain, and stiffness. In addition to these physical symptoms, it is also accompanied by psychological symptoms such as cognitive deficits, anxiety, and depression. One of the non-pharmacological treatments that have been used in this pathology in recent years is neurofeedback. In this study, we analyze the efficacy of sLORETA Neurofeedback in the case of fibromyalgia. The experimental subject was a 37-year-old patient. Quantified electroencephalography studies were applied on three occasions, one initial, another after fifteen days of waiting list, and another after treatment. Psychometric scales were also applied at the same time to evaluate the patient's psychological and physical state. The treatment consisted of 5 sessions of Neurofeedback LORETA in Brodmann area 2. After the treatment, a neurometric, psychometric, and clinical improvement were found. The improvement of the patient after 5 sessions is relevant since previous studies using neurofeedback in fibromyalgia, despite finding positive results, needed a higher number of sessions to achieve relevant results. Therefore, the intervention with neurofeedback LORETA in fibromyalgia patients could be an alternative or complement to current treatments.
{"title":"sLORETA neurofeedback in fibromyalgia","authors":"R. Pérez-Elvira, Ana Jiménez Gómez","doi":"10.31117/NEUROSCIRN.V3I1.40","DOIUrl":"https://doi.org/10.31117/NEUROSCIRN.V3I1.40","url":null,"abstract":"Fibromyalgia is a chronic and incapacitating condition that produces, as main symptoms, pain, and stiffness. In addition to these physical symptoms, it is also accompanied by psychological symptoms such as cognitive deficits, anxiety, and depression. One of the non-pharmacological treatments that have been used in this pathology in recent years is neurofeedback. In this study, we analyze the efficacy of sLORETA Neurofeedback in the case of fibromyalgia. The experimental subject was a 37-year-old patient. Quantified electroencephalography studies were applied on three occasions, one initial, another after fifteen days of waiting list, and another after treatment. Psychometric scales were also applied at the same time to evaluate the patient's psychological and physical state. The treatment consisted of 5 sessions of Neurofeedback LORETA in Brodmann area 2. After the treatment, a neurometric, psychometric, and clinical improvement were found. The improvement of the patient after 5 sessions is relevant since previous studies using neurofeedback in fibromyalgia, despite finding positive results, needed a higher number of sessions to achieve relevant results. Therefore, the intervention with neurofeedback LORETA in fibromyalgia patients could be an alternative or complement to current treatments.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47156350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-12-04DOI: 10.31117/neuroscirn.v2i4.36
Asraa Faris Aldoghachi, P. Cheah, Normala Ibrahim, Munn Sann Lye, K. Ling
Major depressive disorder (MDD) is a serious mental illness with a multifactorial aetiology that was shown to influence behaviour and affect cognition. Previous research has favoured the involvement of dopamine in the aetiology of the disorder, and since one of the critical regulators of the dopamine levels and activity in the brain is DAT1, the present study investigated the association of a single nucleotide polymorphism in the DAT1 gene (rs40184) and MDD in the Malaysian population. A total of 300 cases and 300 matched controls were recruited from four Klang valley hospitals and were screened for DAT1 rs40184 using high resolution melting assays. The allele and genotype frequencies were analysed by using Chi-square. Hardy Weinberg equilibrium for the distribution of alleles and genotypes was tested by using Chi-square. Determination of the association between rs40184 and MDD was achieved by conditional logistic regression using SPSS. In the present study, no significant association was obtained between DAT1 and MDD in the Malaysian population.
{"title":"Dopamine transporter 1 (DAT1) rs40184 single nucleotide polymorphism is not associated with the Malaysian major depressive disorder subjects","authors":"Asraa Faris Aldoghachi, P. Cheah, Normala Ibrahim, Munn Sann Lye, K. Ling","doi":"10.31117/neuroscirn.v2i4.36","DOIUrl":"https://doi.org/10.31117/neuroscirn.v2i4.36","url":null,"abstract":"Major depressive disorder (MDD) is a serious mental illness with a multifactorial aetiology that was shown to influence behaviour and affect cognition. Previous research has favoured the involvement of dopamine in the aetiology of the disorder, and since one of the critical regulators of the dopamine levels and activity in the brain is DAT1, the present study investigated the association of a single nucleotide polymorphism in the DAT1 gene (rs40184) and MDD in the Malaysian population. A total of 300 cases and 300 matched controls were recruited from four Klang valley hospitals and were screened for DAT1 rs40184 using high resolution melting assays. The allele and genotype frequencies were analysed by using Chi-square. Hardy Weinberg equilibrium for the distribution of alleles and genotypes was tested by using Chi-square. Determination of the association between rs40184 and MDD was achieved by conditional logistic regression using SPSS. In the present study, no significant association was obtained between DAT1 and MDD in the Malaysian population.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41894743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-11-19DOI: 10.31117/neuroscirn.v2i4.43
J. Y. Teoh, Kee Hean Lim
‘Working Together to Prevent Suicide’ is the theme of World Mental Health Day 2019. According to the World Health Organisation, suicide is the second leading cause of death for people aged 15-19 years old. One person dies of suicide every 40 seconds, with this form of death affecting people of all age groups in all countries. Hence in line with this year’s theme calling for a trans-sectoral and interdisciplinary approach to address this epidemic, we would like to invite all contributors and readers of Neuroscience Research Notes (NeurosciRN) to take a moment to reflect on how they - as researchers can contribute towards the facilitation, discussion and promotion of positive mental health, which in turn has been found to reduce suicide risk.
{"title":"Research beyond biomedical confines: towards better mental health and well-being for all","authors":"J. Y. Teoh, Kee Hean Lim","doi":"10.31117/neuroscirn.v2i4.43","DOIUrl":"https://doi.org/10.31117/neuroscirn.v2i4.43","url":null,"abstract":"‘Working Together to Prevent Suicide’ is the theme of World Mental Health Day 2019. According to the World Health Organisation, suicide is the second leading cause of death for people aged 15-19 years old. One person dies of suicide every 40 seconds, with this form of death affecting people of all age groups in all countries. Hence in line with this year’s theme calling for a trans-sectoral and interdisciplinary approach to address this epidemic, we would like to invite all contributors and readers of Neuroscience Research Notes (NeurosciRN) to take a moment to reflect on how they - as researchers can contribute towards the facilitation, discussion and promotion of positive mental health, which in turn has been found to reduce suicide risk.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45316253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-13DOI: 10.31117/neuroscirn.v2i3.34
Munn Sann Lye, A. Shahbudin, Yin-Yee Tey, Y. Tor, K. Ling, Normala Ibrahim, J. Stanslas, S. Loh, R. Rosli
Major depressive disorder (MDD) compromises the individual’s capacity for self-care and productivity. Single nucleotide polymorphisms (SNP) of a number of genes have been associated with MDD. The zinc transporter-3 protein, encoded by the ZnT3 (SLC30A3) gene, maintains zinc-glutamate homeostasis at the glutamatergic synapse, a disruption of which increases risk of MDD. We hypothesise that variation in SLC30A3 (rs11126936) SNP increases risk of MDD. We recruited 300 MDD cases and 300 controls, matched in the ratio of 1:1 by age, gender and ethnicity. PCR-restriction fragment length polymorphism analysis was used in DNA genotyping, validated by sequencing 10% of samples. Deviation from the Hardy-Weinberg equilibrium was tested using the chi-square test. Conditional logistic regression was used to estimate adjusted odds ratios, controlling for age, gender, ethnicity, occupation and family monthly income. Genotypes G/G and G/T showed two times greater odds of developing MDD compared to variant genotype T/T (OR=1.983, 95% CI=1.031-3.815; p=0.040 and OR=2.232, 95% CI=1.100-4.533; p=0.026 respectively). Carriers of genotypes G/G and G/T of the SNP rs11126936 in SLC30A3 are associated with increased risk of MDD.
{"title":"Zinc transporter-3 [SLC30A3 (rs11126936)] polymorphism is associated with major depressive disorder in Asian subjects","authors":"Munn Sann Lye, A. Shahbudin, Yin-Yee Tey, Y. Tor, K. Ling, Normala Ibrahim, J. Stanslas, S. Loh, R. Rosli","doi":"10.31117/neuroscirn.v2i3.34","DOIUrl":"https://doi.org/10.31117/neuroscirn.v2i3.34","url":null,"abstract":"Major depressive disorder (MDD) compromises the individual’s capacity for self-care and productivity. Single nucleotide polymorphisms (SNP) of a number of genes have been associated with MDD. The zinc transporter-3 protein, encoded by the ZnT3 (SLC30A3) gene, maintains zinc-glutamate homeostasis at the glutamatergic synapse, a disruption of which increases risk of MDD. We hypothesise that variation in SLC30A3 (rs11126936) SNP increases risk of MDD. We recruited 300 MDD cases and 300 controls, matched in the ratio of 1:1 by age, gender and ethnicity. PCR-restriction fragment length polymorphism analysis was used in DNA genotyping, validated by sequencing 10% of samples. Deviation from the Hardy-Weinberg equilibrium was tested using the chi-square test. Conditional logistic regression was used to estimate adjusted odds ratios, controlling for age, gender, ethnicity, occupation and family monthly income. Genotypes G/G and G/T showed two times greater odds of developing MDD compared to variant genotype T/T (OR=1.983, 95% CI=1.031-3.815; p=0.040 and OR=2.232, 95% CI=1.100-4.533; p=0.026 respectively). Carriers of genotypes G/G and G/T of the SNP rs11126936 in SLC30A3 are associated with increased risk of MDD.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47170539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-08-22DOI: 10.31117/NEUROSCIRN.V2I3.30
R. Bagchi, A. Bagchi, Ankita Salunke, D. Hens, Pragna Parikh
Hypoxia-induced oxidative stress contributes to neuronal damage leading to many neurodegenerative disorders. Hypoxia promotes many downstream effectors such as hypoxia-inducible factor-1α (HIF-1α) in order to restore respiratory homeostasis due to low oxygen availability and increased ROS. Use of histone deacetylase (HDAC) inhibitors may modulate hypoxia-induced neuronal cell damage. In this study, we used two chemically diverse HDAC inhibitors to investigate their effect on hypoxia-exposed neuronal cells. Human pluripotent NT-2 stem cell-derived neuronal differentiated cells were exposed to CoCl2 pre-treatment for 6h to induce hypoxia, prior to supplementation of HDAC inhibitor (SAHA or MGCD0103). Treatment with HDAC inhibitor improved cell viability in hypoxia-induced neuronal cells. The increased HIF1α expression in hypoxia-induced neuronal cells was blunted by these HDAC inhibitors with a concomitant decrease in ROS production. CoCl2 treatment caused an increase in IL-1β, which was significantly inhibited by these HDAC inhibitors. Furthermore, apoptosis induced in these CoCl2 treated neuronal cells was mitigated by SAHA as well MGCD0103 suggesting that these HDAC inhibitors are capable of reducing cellular toxicity, inflammation and apoptosis, and thus, could be beneficial as therapeutic molecules for many neuropathological conditions.
{"title":"Chemical hypoxia in human pluripotent NT2 stem cell-derived neurons: Effect of hydroxamic acid and benzamide-based epigenetic drugs","authors":"R. Bagchi, A. Bagchi, Ankita Salunke, D. Hens, Pragna Parikh","doi":"10.31117/NEUROSCIRN.V2I3.30","DOIUrl":"https://doi.org/10.31117/NEUROSCIRN.V2I3.30","url":null,"abstract":"Hypoxia-induced oxidative stress contributes to neuronal damage leading to many neurodegenerative disorders. Hypoxia promotes many downstream effectors such as hypoxia-inducible factor-1α (HIF-1α) in order to restore respiratory homeostasis due to low oxygen availability and increased ROS. Use of histone deacetylase (HDAC) inhibitors may modulate hypoxia-induced neuronal cell damage. In this study, we used two chemically diverse HDAC inhibitors to investigate their effect on hypoxia-exposed neuronal cells. Human pluripotent NT-2 stem cell-derived neuronal differentiated cells were exposed to CoCl2 pre-treatment for 6h to induce hypoxia, prior to supplementation of HDAC inhibitor (SAHA or MGCD0103). Treatment with HDAC inhibitor improved cell viability in hypoxia-induced neuronal cells. The increased HIF1α expression in hypoxia-induced neuronal cells was blunted by these HDAC inhibitors with a concomitant decrease in ROS production. CoCl2 treatment caused an increase in IL-1β, which was significantly inhibited by these HDAC inhibitors. Furthermore, apoptosis induced in these CoCl2 treated neuronal cells was mitigated by SAHA as well MGCD0103 suggesting that these HDAC inhibitors are capable of reducing cellular toxicity, inflammation and apoptosis, and thus, could be beneficial as therapeutic molecules for many neuropathological conditions.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47488173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-08-17DOI: 10.31117/NEUROSCIRN.V2I3.35
T. Toh, K. Lim, C. Ng, Imran Idris, S. Ahmad, T. Lim, I. Looi, A. Tan, Chung-Kin Chan, C. Lim, C. Tan
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary disease of small cerebral arteries. This case series aims to describe the mutations in NOTCH3 and their phenotypes in Malaysia. We included patients who were genetically confirmed to have CADASIL, diagnosed at the University of Malaya Medical Centre, Malaysia. Family members who fulfilled clinical or imaging criteria, and patients from two previous published Malaysian families were also included. Six families (eleven cases) were included in this series. Genetic testing revealed NOTCH3 mutations in c.328C>T (p.Arg110Cys, R110C), c.533T>G (p.Cys185Gly, C185G), c.1630C>T (p.Arg544Cys, R544C) and c.160C>T (p.Arg54Cys, R54C). Two out of four Chinese families had R544C mutation in exon 11, with a later age of onset, absence of migraine and lack of anterior temporal pole involvement on MRI. One family with mixed Indian and Chinese ancestry had a mutation in exon 3 with R110C and another Indian family exon 4 with C185G mutation. This case series highlights the genotypic and phenotypic variability of CADASIL in a multiethnic country. The finding of p.Arg544Cys mutation among the older Chinese families, similar to those reported in Jeju Island and Taiwan, suggest the need to screen the older Chinese stroke patients with typical MRI changes.
{"title":"Genotypic and phenotypic variation of CADASIL among Chinese, Indians and Rungus in Malaysia","authors":"T. Toh, K. Lim, C. Ng, Imran Idris, S. Ahmad, T. Lim, I. Looi, A. Tan, Chung-Kin Chan, C. Lim, C. Tan","doi":"10.31117/NEUROSCIRN.V2I3.35","DOIUrl":"https://doi.org/10.31117/NEUROSCIRN.V2I3.35","url":null,"abstract":"Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary disease of small cerebral arteries. This case series aims to describe the mutations in NOTCH3 and their phenotypes in Malaysia. We included patients who were genetically confirmed to have CADASIL, diagnosed at the University of Malaya Medical Centre, Malaysia. Family members who fulfilled clinical or imaging criteria, and patients from two previous published Malaysian families were also included. Six families (eleven cases) were included in this series. Genetic testing revealed NOTCH3 mutations in c.328C>T (p.Arg110Cys, R110C), c.533T>G (p.Cys185Gly, C185G), c.1630C>T (p.Arg544Cys, R544C) and c.160C>T (p.Arg54Cys, R54C). Two out of four Chinese families had R544C mutation in exon 11, with a later age of onset, absence of migraine and lack of anterior temporal pole involvement on MRI. One family with mixed Indian and Chinese ancestry had a mutation in exon 3 with R110C and another Indian family exon 4 with C185G mutation. This case series highlights the genotypic and phenotypic variability of CADASIL in a multiethnic country. The finding of p.Arg544Cys mutation among the older Chinese families, similar to those reported in Jeju Island and Taiwan, suggest the need to screen the older Chinese stroke patients with typical MRI changes.","PeriodicalId":36108,"journal":{"name":"Neuroscience Research Notes","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43638501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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