Displaying publications 241 - 260 of 284 in total

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  1. Fulltext REST and Neural Gene Network Dysregulation in iPSC Models of Alzheimer's Disease
    Meyer K, Feldman HM, Lu T, Drake D, Lim ET, Ling KH, et al.
    Cell Rep, 2019 01 29;26(5):1112-1127.e9.
    PMID: 30699343 DOI: 10.1016/j.celrep.2019.01.023
    The molecular basis of the earliest neuronal changes that lead to Alzheimer's disease (AD) is unclear. Here, we analyze neural cells derived from sporadic AD (SAD), APOE4 gene-edited and control induced pluripotent stem cells (iPSCs). We observe major differences in iPSC-derived neural progenitor (NP) cells and neurons in gene networks related to neuronal differentiation, neurogenesis, and synaptic transmission. The iPSC-derived neural cells from SAD patients exhibit accelerated neural differentiation and reduced progenitor cell renewal. Moreover, a similar phenotype appears in NP cells and cerebral organoids derived from APOE4 iPSCs. Impaired function of the transcriptional repressor REST is strongly implicated in the altered transcriptome and differentiation state. SAD and APOE4 expression result in reduced REST nuclear translocation and chromatin binding, and disruption of the nuclear lamina. Thus, dysregulation of neural gene networks may set in motion the pathologic cascade that leads to AD.
    Matched MeSH terms: Neurons/metabolism*
  2. Chronic cerebral hypoperfusion-induced memory impairment and hippocampal long-term potentiation deficits are improved by cholinergic stimulation in rats
    Damodaran T, Müller CP, Hassan Z
    Pharmacol Rep, 2019 Jun;71(3):443-448.
    PMID: 31003155 DOI: 10.1016/j.pharep.2019.01.012
    BACKGROUND: Chronic cerebral hypoperfusion (CCH) can induce the accumulation of reactive oxygen species, which leads to oxidative damage, neuronal injury, and central cholinergic dysfunction in vulnerable regions of the brain, such as the hippocampus and cerebral cortex. These effects can lead to significant cognitive impairments in clinical populations of vascular dementia (VaD). The present studies aimed to investigate the role of the cholinergic system in memory functions and hippocampal long-term potentiation (LTP) impairments induced by CCH in rats.

    METHODS: Male Sprague Dawley rats were subjected to permanent bilateral occlusion of common carotid arteries (PBOCCA) or sham surgery. Then, PBOCCA rats received ip injections with, either vehicle (control group), the muscarinic receptor agonist oxotremorine (0.1 mg/kg), or the acetylcholinesterase inhibitor physostigmine (0.1 mg/kg). Cognitive functions were evaluated using a passive avoidance task and the Morris water maze test. In addition, hippocampal LTP was recorded in vivo under anaesthesia.

    RESULTS: The PBOCCA rats exhibited significant deficits in passive avoidance retention and spatial learning and memory tests. They also showed a suppression of LTP formation in the hippocampus. Oxotremorine and physostigmine significantly improved the learning and memory deficits as well as the suppression of LTP in PBOCCA rats.

    CONCLUSIONS: The present data suggest that the cholinergic system plays an important role in CCH-induced cognitive deficits and could be an effective therapeutic target for the treatment of VaD.

    Matched MeSH terms: Neurons/drug effects
  3. Alleviatory effects of Danshen, Salvianolic acid A and Salvianolic acid B on PC12 neuronal cells and Drosophila melanogaster model of Alzheimer's disease
    Tan FHP, Ting ACJ, Leow BG, Najimudin N, Watanabe N, Azzam G
    J Ethnopharmacol, 2021 Oct 28;279:114389.
    PMID: 34217797 DOI: 10.1016/j.jep.2021.114389
    ETHNOPHARMACOLOGICAL RELEVANCE: Danshen water extract (DWE), obtained from the Salvia miltiorrhiza Bunge (Family Lamiaceae) root, is usually employed in Chinese traditional medicine as treatment to cardiovascular ailments and cerebrovascular diseases. Intriguingly, the extract was also found to contain vast beneficial properties in Alzheimer's disease (AD) treatment.

    AIM OF THE STUDY: Alzheimer's disease is the most significant type of neurodegenerative disorder plaguing societies globally. Its pathogenesis encompasses the hallmark aggregation of amyloid-beta (Aβ). Of all the Aβ oligomers formed in the brain, Aβ42 is the most toxic and aggressive. Despite this, the mechanism behind this disease remains elusive. In this study, DWE, and its major components, Salvianolic acid A (SalA) and Salvianolic acid B (SalB) were tested for their abilities to attenuate Aβ42's toxic effects.

    METHODS: The composition of DWE was determined via Ultra-Performance Liquid Chromatography (UPLC). DWE, SalA and SalB were first verified for their capability to diminish Aβ42 fibrillation using an in vitro activity assay. Since Aβ42 aggregation results in neuronal degeneration, the potential Aβ42 inhibitors were next evaluated on Aβ42-exposed PC12 neuronal cells. The Drosophila melanogaster AD model was then employed to determine the effects of DWE, SalA and SalB.

    RESULTS: DWE, SalA and SalB were shown to be able to reduce fibrillation of Aβ42. When tested on PC12 neuronal cells, DWE, SalA and SalB ameliorated cells from cell death associated with Aβ42 exposure. Next, DWE and its components were tested on the Drosophila melanogaster AD model and their rescue effects were further characterized. The UPLC analysis showed that SalA and SalB were present in the brains and bodies of Drosophila after DWE feeding. When human Aβ42 was expressed, the AD Drosophila exhibited degenerated eye structures known as the rough eye phenotype (REP), reduced lifespan and deteriorated locomotor ability. Administration of DWE, SalA and SalB partially reverted the REP, increased the age of AD Drosophila and improved most of the mobility of AD Drosophila.

    CONCLUSION: Collectively, DWE and its components may have therapeutic potential for AD patients and possibly other forms of brain diseases.

    Matched MeSH terms: Neurons/drug effects*
  4. Fulltext Neuroprotective effects of alpha lipoic Acid on haloperidol-induced oxidative stress in the rat brain
    Perera J, Tan JH, Jeevathayaparan S, Chakravarthi S, Haleagrahara N
    Cell Biosci, 2011;1(1):12.
    PMID: 21711768 DOI: 10.1186/2045-3701-1-12
    Haloperidol is an antipsychotic drug that exerts its' antipsychotic effects by inhibiting dopaminergic neurons. Although the exact pathophysiology of haloperidol extrapyramidal symptoms are not known, the role of reactive oxygen species in inducing oxidative stress has been proposed as one of the mechanisms of prolonged haloperidol-induced neurotoxicity. In the present study, we evaluate the protective effect of alpha lipoic acid against haloperidol-induced oxidative stress in the rat brain. Sprague Dawley rats were divided into control, alpha lipoic acid alone (100 mg/kg p.o for 21 days), haloperidol alone (2 mg/kg i.p for 21 days), and haloperidol with alpha lipoic acid groups (for 21 days). Haloperidol treatment significantly decreased levels of the brain antioxidant enzymes super oxide dismutase and glutathione peroxidase and concurrent treatment with alpha lipoic acid significantly reversed the oxidative effects of haloperidol. Histopathological changes revealed significant haloperidol-induced damage in the cerebral cortex, internal capsule, and substantia nigra. Alpha lipoic acid significantly reduced this damage and there were very little neuronal atrophy. Areas of angiogenesis were also seen in the alpha lipoic acid-treated group. In conclusion, the study proves that alpha lipoic acid treatment significantly reduces haloperidol-induced neuronal damage.
    Matched MeSH terms: Dopaminergic Neurons
  5. Fulltext Aging and chronic administration of serotonin-selective reuptake inhibitor citalopram upregulate Sirt4 gene expression in the preoptic area of male mice
    Wong DW, Soga T, Parhar IS
    Front Genet, 2015;6:281.
    PMID: 26442099 DOI: 10.3389/fgene.2015.00281
    Sexual dysfunction and cognitive deficits are markers of the aging process. Mammalian sirtuins (SIRT), encoded by sirt 1-7 genes, are known as aging molecules which are sensitive to serotonin (5-hydroxytryptamine, 5-HT). Whether the 5-HT system regulates SIRT in the preoptic area (POA), which could affect reproduction and cognition has not been examined. Therefore, this study was designed to examine the effects of citalopram (CIT, 10 mg/kg for 4 weeks), a potent selective-serotonin reuptake inhibitor and aging on SIRT expression in the POA of male mice using real-time PCR and immunocytochemistry. Age-related increases of sirt1, sirt4, sirt5, and sirt7 mRNA levels were observed in the POA of 52 weeks old mice. Furthermore, 4 weeks of chronic CIT treatment started at 8 weeks of age also increased sirt2 and sirt4 mRNA expression in the POA. Moreover, the number of SIRT4 immuno-reactive neurons increased with aging in the medial septum area (12 weeks = 1.00 ± 0.15 vs. 36 weeks = 1.68 ± 0.14 vs. 52 weeks = 1.54 ± 0.11, p < 0.05). In contrast, the number of sirt4-immunopositive cells did not show a statistically significant change with CIT treatment, suggesting that the increase in sirt4 mRNA levels may occur in cells in which sirt4 is already being expressed. Taken together, these studies suggest that CIT treatment and the process of aging utilize the serotonergic system to up-regulate SIRT4 in the POA as a common pathway to deregulate social cognitive and reproductive functions.
    Matched MeSH terms: Neurons
  6. Fulltext Neural Differentiation of Human Pluripotent Stem Cells for Nontherapeutic Applications: Toxicology, Pharmacology, and In Vitro Disease Modeling
    Yap MS, Nathan KR, Yeo Y, Lim LW, Poh CL, Richards M, et al.
    Stem Cells Int, 2015;2015:105172.
    PMID: 26089911 DOI: 10.1155/2015/105172
    Human pluripotent stem cells (hPSCs) derived from either blastocyst stage embryos (hESCs) or reprogrammed somatic cells (iPSCs) can provide an abundant source of human neuronal lineages that were previously sourced from human cadavers, abortuses, and discarded surgical waste. In addition to the well-known potential therapeutic application of these cells in regenerative medicine, these are also various promising nontherapeutic applications in toxicological and pharmacological screening of neuroactive compounds, as well as for in vitro modeling of neurodegenerative and neurodevelopmental disorders. Compared to alternative research models based on laboratory animals and immortalized cancer-derived human neural cell lines, neuronal cells differentiated from hPSCs possess the advantages of species specificity together with genetic and physiological normality, which could more closely recapitulate in vivo conditions within the human central nervous system. This review critically examines the various potential nontherapeutic applications of hPSC-derived neuronal lineages and gives a brief overview of differentiation protocols utilized to generate these cells from hESCs and iPSCs.
    Matched MeSH terms: Neurons
  7. Fulltext Treatment of spinal cord injury with mesenchymal stem cells
    Liau LL, Looi QH, Chia WC, Subramaniam T, Ng MH, Law JX
    Cell Biosci, 2020;10:112.
    PMID: 32983406 DOI: 10.1186/s13578-020-00475-3
    Background: Spinal cord injury (SCI) is the damage to the spinal cord that can lead to temporary or permanent loss of function due to injury to the nerve. The SCI patients are often associated with poor quality of life.

    Results: This review discusses the current status of mesenchymal stem cell (MSC) therapy for SCI, criteria to considering for the application of MSC therapy and novel biological therapies that can be applied together with MSCs to enhance its efficacy. Bone marrow-derived MSCs (BMSCs), umbilical cord-derived MSCs (UC-MSCs) and adipose tissue-derived MSCs (ADSCs) have been trialed for the treatment of SCI. Application of MSCs may minimize secondary injury to the spinal cord and protect the neural elements that survived the initial mechanical insult by suppressing the inflammation. Additionally, MSCs have been shown to differentiate into neuron-like cells and stimulate neural stem cell proliferation to rebuild the damaged nerve tissue.

    Conclusion: These characteristics are crucial for the restoration of spinal cord function upon SCI as damaged cord has limited regenerative capacity and it is also something that cannot be achieved by pharmacological and physiotherapy interventions. New biological therapies including stem cell secretome therapy, immunotherapy and scaffolds can be combined with MSC therapy to enhance its therapeutic effects.

    Matched MeSH terms: Neurons
  8. Neuropsychiatric implications of transient receptor potential vanilloid (TRPV) channels in the reward system
    Singh R, Bansal Y, Parhar I, Kuhad A, Soga T
    Neurochem Int, 2019 12;131:104545.
    PMID: 31494132 DOI: 10.1016/j.neuint.2019.104545
    Neuropsychiatric disorders (NPDs) exert a devastating impact on an individual's personal and social well-being, encompassing various conditions and brain anomalies that influence affect, cognition, and behavior. Because the pathophysiology of NPDs is multifactorial, the precise mechanisms underlying the development of such disorders remain unclear, representing a unique challenge in current neuropsychopharmacotherapy. Transient receptor potential vanilloid (TRPV) type channels are a family of ligand-gated ion channels that mainly include sensory receptors that respond to thermal, mechanical and chemical stimuli. TRPV channels are abundantly present in dopaminergic neurons, thus playing a pivotal role in the modulation of the reward system and in pathophysiology of diseases such as stress, anxiety, depression, schizophrenia, neurodegenerative disorders and substance abuse/addiction. Recent evidence has highlighted TRPV channels as potential targets for understanding modulation of the reward system and various forms of addiction (opioids, cocaine, amphetamines, alcohol, nicotine, cannabis). In this review, we discuss the distribution, physiological roles, ligands and therapeutic importance of TRPV channels with regard to NPDs and addiction biology.
    Matched MeSH terms: Dopaminergic Neurons
  9. Fulltext Deciphering Direct and Indirect Effects of Neurokinin B and GnRH in the Brain-Pituitary Axis of Tilapia
    Mizrahi N, Gilon C, Atre I, Ogawa S, Parhar IS, Levavi-Sivan B
    Front Endocrinol (Lausanne), 2019;10:469.
    PMID: 31354632 DOI: 10.3389/fendo.2019.00469
    Neurokinin B (NKB) and its cognate receptor (NK3R) are emerging as important components of the neuroendocrine regulation of reproduction. Unlike mammalian tac3, which encodes only one mature peptide (namely NKB), two mature peptides are predicted for each tac3 gene in fish and frogs. Therefore, it was designated as Neurokinin F (NKF). Hormone analogs with high and long-lasting biological activity are important tools for physiological and biological research; however, the availability of piscine-specific analogs is very limited. Therefore, we have developed specific NKB and NKF analogs based on the structure of the mammalian NKB analog-senktide. These analogs, specifically designed for longer half-lives by methylation of proteolysis sites, exhibited activity equal to those of the native NKB and NKF in short-term signal-transduction assays of tilapia NKB receptors. However, the analogs were found to be able to significantly increase the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and growth hormone (GH) in tilapia, as fast as 1 h after intraperitoneal (IP) injection. The impact of the analogs on LH and FSH secretion lasted longer compared to the effect of native peptides and salmon GnRH analog (sGnRHa). In addition, we harvested pituitaries 24 h post injection and measured LH, FSH and GH mRNA synthesis. Both analogs elevated mRNA levels of LH and GH, but only NKB analog increased FSH mRNA levels in the pituitary and all GnRH forms in the brain. NKB receptors were co-localized with all three types the GnRH neurons in tilapia brain in situ. We previously showed a direct effect of NKB at the pituitary level, and these new results suggest that the stronger impact of the NKB analog on GTH release is also due to an indirect effect through the activation of GnRH neurons. These results suggest that novel synthetic NKB analogs may serve as a tool for both research and agricultural purposes. Finally, the biological activity and regulatory role of NKB in tilapia brain and pituitary suggest that the NKB/NKBR system in fish is an important reproductive regulator in a similar way to the kisspeptin system in mammals.
    Matched MeSH terms: Neurons
  10. Incremental benefits of EEG informed fMRI in the study of disorders related to meso-corticolimbic dopamine pathway dysfunction: A systematic review of recent literature
    Syed Nasser N, Ibrahim B, Sharifat H, Abdul Rashid A, Suppiah S
    J Clin Neurosci, 2019 Jul;65:87-99.
    PMID: 30955950 DOI: 10.1016/j.jocn.2019.03.054
    Functional magnetic resonance imaging (fMRI) is a non-invasive imaging modality that enables the assessment of neural connectivity and oxygen utility of the brain using blood oxygen level dependent (BOLD) imaging sequence. Electroencephalography (EEG), on the other hands, looks at cortical electrical impulses of the brain thus detecting brainwave patterns during rest and thought processing. The combination of these two modalities is called fMRI with simultaneous EEG (fMRI-EEG), which has emerged as a new tool for experimental neuroscience assessments and has been applied clinically in many settings, most commonly in epilepsy cases. Recent advances in imaging has led to fMRI-EEG being utilized in behavioural studies which can help in giving an objective assessment of ambiguous cases and help in the assessment of response to treatment by providing a non-invasive biomarker of the disease processes. We aim to review the role and interpretation of fMRI-EEG in studies pertaining to psychiatric disorders and behavioral abnormalities.
    Matched MeSH terms: Dopaminergic Neurons
  11. Fulltext Effects of Tualang honey on pain behaviour and oxidative stress in the thalamus of prenatally stressed rat offspring
    Hidani Hasim, Che Badariah Abd Aziz, Siti Qusyasyiah Ahmad Suhaimi, Mahaneem Mohamed, Idris Long, Rahimah Zakaria
    Malaysian Journal of Medicine and Health Sciences, 2020;16(3):85-92.
    MyJurnal
    Introduction: Increased nociceptive responses were shown in the offspring of prenatally stressed rats. Reports have demonstrated the anti-nociceptive effects of Tualang honey in the rat offspring. The present study was done to de- termine whether the modulation of nociceptive behaviour by Tualang honey was mediated by modulating changes in the histology, oxidative stress parameters and N-methyl-D-aspartate (NMDA) receptors in the thalamus of the rat offspring. Methods: Eighteen Sprague Dawley pregnant rats were randomly assigned to control (C), stress (S) and stress-treated with Tualang honey (SH) groups. Stress was given in a form of restraint stress.Tualang honey was given to SH group from first day of pregnancy until delivery. Thirty-three adult male offspring were subjected to formalin test before they were sacrificed. Nociceptive behaviour score, number of neurons, level of oxidative stress parameters and NMDA receptors in the thalamus were analysed by using one-way ANOVA. Results: The study demonstrated a significant decrease in mean nociceptive behaviour score (p
    Matched MeSH terms: Neurons
  12. Fulltext MicroRNA Dysregulation in Parkinson's Disease: A Narrative Review
    Nies YH, Mohamad Najib NH, Lim WL, Kamaruzzaman MA, Yahaya MF, Teoh SL
    Front Neurosci, 2021;15:660379.
    PMID: 33994934 DOI: 10.3389/fnins.2021.660379
    Parkinson's disease (PD) is a severely debilitating neurodegenerative disease, affecting the motor system, leading to resting tremor, cogwheel rigidity, bradykinesia, walking and gait difficulties, and postural instability. The severe loss of dopaminergic neurons in the substantia nigra pars compacta causes striatal dopamine deficiency and the presence of Lewy bodies indicates a pathological hallmark of PD. Although the current treatment of PD aims to preserve dopaminergic neurons or to replace dopamine depletion in the brain, it is notable that complete recovery from the disease is yet to be achieved. Given the complexity and multisystem effects of PD, the underlying mechanisms of PD pathogenesis are yet to be elucidated. The advancement of medical technologies has given some insights in understanding the mechanism and potential treatment of PD with a special interest in the role of microRNAs (miRNAs) to unravel the pathophysiology of PD. In PD patients, it was found that striatal brain tissue and dopaminergic neurons from the substantia nigra demonstrated dysregulated miRNAs expression profiles. Hence, dysregulation of miRNAs may contribute to the pathogenesis of PD through modulation of PD-associated gene and protein expression. This review will discuss recent findings on PD-associated miRNAs dysregulation, from the regulation of PD-associated genes, dopaminergic neuron survival, α-synuclein-induced inflammation and circulating miRNAs. The next section of this review also provides an update on the potential uses of miRNAs as diagnostic biomarkers and therapeutic tools for PD.
    Matched MeSH terms: Dopaminergic Neurons
  13. Fulltext An inhibited dopamine synthesizing cell model of AADC deficiency
    Melati Khalid, Mohamad Aris Mohd Moklas
    Life Sciences, Medicine and Biomedicine, 2019;3(2):1-7.
    MyJurnal
    Aromatic L-amino acid decarboxylase deficiency (AADC) is a rare autosomal recessive pediatric neurotransmitter disease. To date it remains poorly understood mainly due to an absence of a disease model. The dopaminergic neuroblastoma cell SH-SY5Y was chosen to develop our AADC deficiency model. These cells are not native dopamine synthesizers. Objective: To develop a dopamine-producing cellular model of AADC deficiency using SH-SY5Y neuroblastoma cells. Methods: Dopamine pathway proteins were identified with Western Blotting. Dopaminergic differentiation was attempted using all-trans retinoic acid (ATRA) with dopamine detection via HPLC-ECD post alumina extraction. Treatment with L-DOPA provided SH-SY5Y with excess precursor. RT-PCR was used to determine the expression of markers of mature neurons. Results: Western Blot screening identified AADC, dopamine β-hydroxylase and tyrosine hyrdoxylase proteins, indicative of a dopaminergic pathway. ATRA was unsuccessful in producing dopamine from the cells. L-DOPA treatment however, generated dopamine first visible as a HPLC-ECD peak 30 minutes post-incubation. Prior to this, SH-SY5Y dopamine synthesis from L-DOPA has never been documented. This de novo synthesis is then inhibited using benserazide to form our AADC deficiency cell model. RT-PCR showed that SH-SY5Y cells express markers of mature neurons in its ‘native’ state and is not affected by L-DOPA and benserazide treatment. This cell model will potentially benefit many areas of AADC deficiency research. Conclusion: SH-SY5Y cells produced HPLC-ECD measureable amounts of dopamine with the addition of L-DOPA. Our model of AADC deficiency is generated by quelling the dopamine production with Benserazide.
    Matched MeSH terms: Dopaminergic Neurons
  14. Fulltext Pathological findings in a mouse model for Coxsackievirus A16 infection
    Hooi, Yuan Teng, Ong, Kien Chai, Perera, David, Wong, Kum Thong
    Neurology Asia, 2015;20(4):343-347.
    MyJurnal
    Coxsackievirus A16 (CV-A16) is the leading cause of hand-foot-mouth disease (HFMD), which usually
    presents as mild and self-limiting symptoms in young children. Rarely, CV-A16 has been reported
    to cause severe and fatal neurological complications but little is known about these complications.
    In the present study, 1-day and 7-day old mouse models of CV-A16 were developed using a clinical
    strain via subcutaneous inoculation. All infected mice exhibited clinical signs of infection, including
    reduced mobility, limb weakness and paralysis between 3 to 6 days post-infection. Pathologically,
    the main organs involved were the central nervous system (CNS), skeletal muscles and brown fat. In
    the CNS, viral antigens as demonstrated by immunohistochemistry, were localized mainly to neurons
    in the brain stem and spinal cord, suggesting that CV-A16 is neurotropic although inflammation is
    very mild. The skeletal muscles showed necrosis and myositis due to viral infection as evidenced by
    the dense viral antigens. Focal viral antigens were also detected in the brown fat. These preliminary
    pathological findings indicate that our mouse models can be further developed to be useful models
    for pathogenesis studies, and vaccine and anti-viral drug evaluation.
    Matched MeSH terms: Neurons
  15. Fulltext Maternal Dexamethasone Exposure Alters Synaptic Inputs to Gonadotropin-Releasing Hormone Neurons in the Early Postnatal Rat
    Lim WL, Idris MM, Kevin FS, Soga T, Parhar IS
    Front Endocrinol (Lausanne), 2016;7:117.
    PMID: 27630615 DOI: 10.3389/fendo.2016.00117
    Maternal dexamethasone [(DEX); a glucocorticoid receptor agonist] exposure delays pubertal onset and alters reproductive behavior in the adult offspring. However, little is known whether maternal DEX exposure affects the offspring's reproductive function by disrupting the gonadotropin-releasing hormone (GnRH) neuronal function in the brain. Therefore, this study determined the exposure of maternal DEX on the GnRH neuronal spine development and synaptic cluster inputs to GnRH neurons using transgenic rats expressing enhanced green fluorescent protein (EGFP) under the control of GnRH promoter. Pregnant females were administered with DEX (0.1 mg/kg) or vehicle (VEH, water) daily during gestation day 13-20. Confocal imaging was used to examine the spine density of EGFP-GnRH neurons by three-dimensional rendering and synaptic cluster inputs to EGFP-GnRH neurons by synapsin I immunohistochemistry on postnatal day 0 (P0) males. The spine morphology and number on GnRH neurons did not change between the P0 males following maternal DEX and VEH treatment. The number of synaptic clusters within the organum vasculosum of the lamina terminalis (OVLT) was decreased by maternal DEX exposure in P0 males. Furthermore, the number and levels of synaptic cluster inputs in close apposition with GnRH neurons was decreased following maternal DEX exposure in the OVLT region of P0 males. In addition, the postsynaptic marker molecule, postsynaptic density 95, was observed in GnRH neurons following both DEX and VEH treatment. These results suggest that maternal DEX exposure alters neural afferent inputs to GnRH neurons during early postnatal stage, which could lead to reproductive dysfunction during adulthood.
    Matched MeSH terms: Neurons
  16. Natural Products Combating Neurodegeneration: Parkinson's Disease
    Solayman M, Islam MA, Alam F, Khalil MI, Kamal MA, Gan SH
    Curr Drug Metab, 2017;18(1):50-61.
    PMID: 27396919 DOI: 10.2174/1389200217666160709204826
    Parkinson's disease (PD) is characterized by neurodegeneration and a progressive functional impairment of the midbrain nigral dopaminergic neurons. The cause remains unknown; however, several pathological processes and central factors, such as protein aggregation, mitochondrial dysfunction, iron accumulation, neuroinflammation and oxidative stress, have been reported. The current treatment method primarily targets symptoms by using anti-Parkinson drugs such as levodopa, carbidopa, dopamine (DA) agonists, monoamine oxidase type B inhibitors and anticholinergics to replace DA. When drug therapy is not satisfactory, surgical treatments are recommended. Unfortunately, the existing conventional strategies that target PD are associated with numerous side effects and possess an economic burden. Therefore, novel therapeutic approaches that regulate the pathways leading to neuronal death and dysfunction are necessary. For many years, nature has provided the primary resource for the discovery of potential therapeutic agents. Remarkably, many natural products from medicinal plants, fruits and vegetables have been demonstrated to be efficacious anti-Parkinson agents. These products possess neuroprotective properties as a result of not only their wellrecognized anti-oxidative and anti-inflammatory activities but also their inhibitory roles regarding iron accumulation, protein misfolding and the maintenance of proteasomal degradation, as well as mitochondrial homeostasis. The aim of this review is to report the available anti-Parkinson agents based on natural products and delineate their therapeutic actions, which act on various pathways. Overall, this review emphasizes the types of natural products that are potential future resources in the treatment of PD as novel regimens or supplementary agents.
    Matched MeSH terms: Dopaminergic Neurons
  17. Glutamate receptors and transporters as comparative cues to the glutamatergic circuits of the avian and mammalian brain
    Islam, M.R., Muzaimi, M., Abdullah, J.M.
    Orient Neuron Nexus, 2011;2(1):2-9.
    MyJurnal
    Glutamate is the principal excitatory neurotransmitter in the central nervous system, and plays important roles in both physiological and pathological neuronal processes. Current understanding of the exact mechanisms involved in glutamate-induced neuronal excitotoxicity, in which excessive glutamate causes neuronal dysfunction and degeneration, whether acute or chronic, remain elusive. Conditions, due to acute insults such as ischaemia and traumatic brain injury, and chronic neurodegenerative disorders such as multiple sclerosis and motor neuron disease, suffer from the lack of translational neuroprotection in clinical setting to tackle glutamate excitotoxicity despite steady growth of animal studies that revealed complex cell death pathway interactions. In addition, glutamates are also released by non-neuronal cells including astrocytes and oligodendroglia. Thus, attempts to elucidate this complexity are closely related to our understanding of the glutamatergic circuitry in the brain. Neuronal cells develop a glutamatergic system at glutamatergic synapses that utilise glutamate as an intercellular signaling molecule to characterise the output, input, and termination of this signaling. As to signal input, various kinds of glutamate receptors have been identified and characterized. Na+-dependent glutamate transporters at the plasma membrane are responsible for the signal termination through sequestration of glutamate from the synaptic cleft. The signal output systems comprise vesicular storage and subsequent exocytosis of glutamate by using vesicular glutamate transporters. Similar to the mammalian brain, the regional differences of glutamatergic neurons and glutamate receptor neurons suggest many glutamatergic projections in the avian brain, as supported by recent evidence of glutamate-related genes distribution. Glutamatergic target areas are expected to show high activity of glutamate transporters that remove released glutamate from the synaptic clefts. This review summarises and compares glutamatergic circuits in the avian and mammalian brain, particularly in the olfactory pathway, the paffial organization of glutamatergic neurons and connection with the striatum, hippocampal-septal pathway, visual and auditory pathways, and granule cell-Purkinje cell pathway in the cerebellum. Comparative appreciation of these glutamatergic circuits, particularly with the localisation and/or expression of specific subtypes of glutamate transporters, would provide the morphological basis for physiological and pharmacological designs that supplement existing animal studies of the current proposed mechanisms that underlie glutamate-induced neuronal excitotoxicity.
    Matched MeSH terms: Neurons
  18. Deep learning for healthcare applications based on physiological signals: A review
    Faust O, Hagiwara Y, Hong TJ, Lih OS, Acharya UR
    Comput Methods Programs Biomed, 2018 Jul;161:1-13.
    PMID: 29852952 DOI: 10.1016/j.cmpb.2018.04.005
    BACKGROUND AND OBJECTIVE: We have cast the net into the ocean of knowledge to retrieve the latest scientific research on deep learning methods for physiological signals. We found 53 research papers on this topic, published from 01.01.2008 to 31.12.2017.

    METHODS: An initial bibliometric analysis shows that the reviewed papers focused on Electromyogram(EMG), Electroencephalogram(EEG), Electrocardiogram(ECG), and Electrooculogram(EOG). These four categories were used to structure the subsequent content review.

    RESULTS: During the content review, we understood that deep learning performs better for big and varied datasets than classic analysis and machine classification methods. Deep learning algorithms try to develop the model by using all the available input.

    CONCLUSIONS: This review paper depicts the application of various deep learning algorithms used till recently, but in future it will be used for more healthcare areas to improve the quality of diagnosis.

    Matched MeSH terms: Neurons
  19. Fulltext Facial nerve palsy in a child: Bell’s palsy? Think again!
    Jo Ee Sam, Nasser Abdul Wahab, Priya Sharda
    Malays Fam Physician, 2017;12(3):30-32.
    MyJurnal
    Introduction: Half of facial paralysis in children is idiopathic at origin. However, dismissing facial
    paralysis as being idiopathic without a thorough history and meticulous examination could be
    disastrous as illustrated by this case.

    Case report: We report a case of sphenoid wing meningioma in a 4-year-old girl. She first
    presented with only facial asymmetry that was noticed by her mother. Examination suggested a
    left upper motor neuron facial nerve palsy. A sphenoid wing meningioma was found on magnetic
    resonance imaging (MRI) of her brain. She underwent craniotomy and total tumour excision.
    Histopathological examination of the tumour showed a grade 1 transitional type meningioma.
    Meningiomas in children are rare compared to the adult population. Presentations in children
    may be delayed due to their inability to recognise or communicate abnormalities. Distinguishing
    between upper and lower motor neuron facial palsy is crucial in decision making for facial paralysis
    in children.
    Matched MeSH terms: Motor Neurons
  20. Ghrelin stimulates growth hormone release from the pituitary via hypothalamic growth hormone-releasing hormone neurons in the cichlid, Oreochromis niloticus
    Ogawa S, Liu X, Shepherd BS, Parhar IS
    Cell Tissue Res, 2018 Nov;374(2):349-365.
    PMID: 29934855 DOI: 10.1007/s00441-018-2870-6
    Ghrelin, a gut-brain peptide hormone, is implicated in a multiplicity of biological functions, including energy homeostasis and reproduction. Neuronal systems that are involved in energy homeostasis as well as reproduction traverse the hypothalamus; however, the mechanism by which they control energy homeostasis is not fully understood. The present study analyzes the anatomical relationship of neurons expressing gonadotropin-releasing hormone (GnRH), neuropeptide Y (NPY) and growth hormone-releasing hormone (GHRH) in a cichlid, tilapia (Oreochromis niloticus). Additionally, we examine in vivo effects of ghrelin on these hypothalamic neurons and plasma growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels. Double-immunofluorescence showed neuronal fiber associations between GnRH, NPY and GHRH in the brain and pituitary. Intracerebroventricular injection of ghrelin had no effect on numbers, soma size, or optical density of GnRH and NPY neurons, whereas the number of GHRH neurons was significantly decreased in the animals injected with ghrelin when compared to controls, which may indicate administered ghrelin promoted GHRH release. Plasma GH and pituitary GH mRNA levels were significantly increased in the animals injected with ghrelin. These results suggest that central administration of ghrelin primarily act on hypothalamic GHRH neurons to stimulate GH release from the pituitary in the tilapia.
    Matched MeSH terms: Neurons
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