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  1. Fulltext Analisis data pengimejan resonans magnet kefungsian: pra pemprosesan ruang menggunakan kaedah pemetaan statistik berparameter
    Ahmad Nazlim Yusoff, Mohd Harith Hashim, Mohd Mahadir Ayob, Iskandar Kassim
    Jurnal Sains Kesihatan Malaysia, 2006;4(1):21-36.
    MyJurnal
    Kajian garis pangkal pengimejan resonans magnet kefungsian (fMRI) telah dijalankan ke atas 2 orang subjek lelaki sihat (kidal dan tidak kidal) masing-masing berumur 22 dan 25 tahun. Imbasan fMRI dijalankan menggunakan sistem pengimejan resonans magnet (MRI) 1.5 T di Jabatan Radiologi, Hospital Universiti Kebangsaan Malaysia. Kajian ini menggunakan gerakanjari tangan kanan dan kiri untuk merangsang aktiviti neuron di dalam korteks serebrum. Paradigma 5 kitar aktifIrehat digunakan dengan setiap kitar mengandungi satu blok aktif dan satu blok rehat yang masing-masing mengandungi 10 siri pengukuran. Imej fMRI dianalisis menggunakan pekej perisian MatLab dan pemetaan statistik berparameter 2 (sPM2). Proses pendaftaran jasad tegar menggunakan penjelmaan afin 6 parameter dilakukan ke atas kesemua imej kefungsian berwajaran T2*. Keputusan menunjukkan bahawa pergerakan subjek adalah minimum sama ada dalam arah translasi (< 1 mm) atau putaran (< 1 ). Kesemua imej dinormalkan melalui proses peledingan tak linear menggunakan penjelmaan afin 12 parameter dan didapati sepadan dengan pencontoh yang telahpun mematuhi ruang anatomi piawai. Walau bagaimanapun, bentuk, resolusi dan kontras imej kefungsian telah berubah sedikit berbanding dengan imej asal. Pelicinan imej menggunakan kernel Gaussian isotropik 6 mm menyebabkan data imej lebih bersifat parametrik dengan kehilangan yang ketara dalam resolusi dan kontras. Pengasingan struktur yang dilakukan ke atas imej berwajaran T1 mengklaskan tisu otak kepadajirim kelabu, jirim putih dan bendalir serebrospina. Pasca pemprosesan ruang bagi imej kefungsian dan struktur menjadikan data imej bersifat parametrik dengan taburan jenis Gaussian dan sedia untuk dianalisis menggunakan model linear am dan teori medan rawak Gaussian.
    Matched MeSH terms: Neurons
  2. Fulltext Pengimejan resonans magnet kefungsian: pemerolehan, analisis dan pentafsiran data
    Ahmad Nazlim Yusoff, Mohd Harith Hashim, Mohd Mahadir Ayob, Iskandar Kassim
    Jurnal Sains Kesihatan Malaysia, 2005;3(2):19-37.
    MyJurnal
    Kajian garis pangkal pengimejan resonans magnet kefungsian (fMRI) telah dijalankan di Jabatan Radiologi, Hospital Universiti Kebangsaan Malaysia ke atas seorang subjek lelaki sihat berumur 25 tahun menggunakan sistem pengimejan resonans magnet (MRI) 1.5 T. Kajian ini menggunakan gerakan jari tangan kanan dan kiri untuk merangsang aktiviti neuron di dalam korteks serebrum. Subjek diarahkan supaya menekan jari-jari pada ibu jari secara bergilir-gilir semasa imbasan kefungsian dilakukan. Paradigma 5 kitar aktifrehat digunakan dengan setiap kitar masing-masing mengandungi 20 siri pengukuran. Keputusan menunjukkan bahawa rantau otak yang aktif akibat gerakan jari adalah girus presentral merangkumi kawasan motor primer. Pengaktifan otak adalah secara kontralateral terhadap gerakan jari tangan kanan dan kiri. Keamatan isyarat keadaan aktif didapati lebih tinggi daripada keamatan isyarat keadaan rehat. Analisis yang dilakukan ke atas beberapa rantau pengaktifan yang diminati (ROI) pada beberapa hirisan menunjukkan perbezaan yang bererti (p < 0.05) antara keamatan keadaan aktif dan rehat untuk nilai ambang statistik (Z) = 1.0 dan 1.5. Perbezaan purata antara kedua-dua purata keamatan isyarat keadaan aktif dan rehat pada manamana hirisan untuk kedua-dua nilai Z menunjukkan magnitud pengaktifan yang lebih tinggi pada hemisfera kanan otak iaitu apabila subjek menggerakkan tangan kirinya. Bilangan voksel yang aktif juga didapati lebih tinggi pada hemisfera kanan berbanding pada hemisfera kiri otak. Keputusan ini menyokong fakta bahawa bagi subjek yang tidak kidal, kawasan pengaktifan motor pada hemisfera kanan otak semasa gerakan jari tangan kiri mengalami rangsangan hemodinamik yang lebih tinggi berbanding dengan hemisfera kiri otak semasa gerakan jari tangan kanan. Fenomena rangsangan hemodinamik yang diperhatikan dalam kajian ini dibincangkan berdasarkan kepada kebergantungan kontras isyarat kepada aras oksigen darah (BOLD).
    Matched MeSH terms: Neurons
  3. Fulltext Artificial neural network with Taguchi method for robust classification model to improve classification accuracy of breast cancer
    Rahman MA, Muniyandi RC, Albashish D, Rahman MM, Usman OL
    PeerJ Comput Sci, 2021;7:e344.
    PMID: 33816995 DOI: 10.7717/peerj-cs.344
    Artificial neural networks (ANN) perform well in real-world classification problems. In this paper, a robust classification model using ANN was constructed to enhance the accuracy of breast cancer classification. The Taguchi method was used to determine the suitable number of neurons in a single hidden layer of the ANN. The selection of a suitable number of neurons helps to solve the overfitting problem by affecting the classification performance of an ANN. With this, a robust classification model was then built for breast cancer classification. Based on the Taguchi method results, the suitable number of neurons selected for the hidden layer in this study is 15, which was used for the training of the proposed ANN model. The developed model was benchmarked upon the Wisconsin Diagnostic Breast Cancer Dataset, popularly known as the UCI dataset. Finally, the proposed model was compared with seven other existing classification models, and it was confirmed that the model in this study had the best accuracy at breast cancer classification, at 98.8%. This confirmed that the proposed model significantly improved performance.
    Matched MeSH terms: Neurons
  4. Identification of blood-based biomarkers for diagnosis and prognosis of Parkinson's disease: A systematic review of proteomics studies
    Chelliah SS, Bhuvanendran S, Magalingam KB, Kamarudin MNA, Radhakrishnan AK
    Ageing Res Rev, 2022 01;73:101514.
    PMID: 34798300 DOI: 10.1016/j.arr.2021.101514
    Parkinson's Disease (PD), a neurodegenerative disorder, is characterised by the loss of motor function and dopamine neurons. Therapeutic avenues remain a challenge due to lack of accuracy in early diagnosis, monitoring of disease progression and limited therapeutic options. Proteomic platforms have been utilised to discover biomarkers for numerous diseases, a tool that may benefit the diagnosis and monitoring of disease progression in PD patients. Therefore, this systematic review focuses on analysing blood-based candidate biomarkers (CB) identified via proteomics platforms for PD. This study systematically reviewed articles across six databases (EMBASE, Cochrane, Ovid Medline, Scopus, Science Direct and PubMed) published between 2010 and 2020. Of the 504 articles identified, 12 controlled-PD studies were selected for further analysis. A total of 115 candidate biomarkers (CB) were identified across selected 12-controlled studies, of which 23 CB were found to be replicable in more than two cohorts. Using the PANTHER Go-Slim classification system and STRING network, the gene function and protein interactions between biomarkers were analysed. Our analysis highlights Apolipoprotein A-I (ApoA-I), which is essential in lipid metabolism, oxidative stress, and neuroprotection demonstrates high replicability across five cohorts with consistent downregulation across four cohorts. Since ApoA-I was highly replicable across blood fractions, proteomic platforms and continents, its relationship with cholesterol, statin and oxidative stress as PD biomarker, its role in the pathogenesis of PD is discussed in this paper. The present study identified ApoA-I as a potential biomarker via proteomics analysis of PD for the early diagnosis and prediction of disease progression.
    Matched MeSH terms: Dopaminergic Neurons
  5. Fulltext Stem cell therapy in neurodegenerative diseases: From principles to practice
    Sakthiswary R, Raymond AA
    Neural Regen Res, 2012 Aug 15;7(23):1822-31.
    PMID: 25624807 DOI: 10.3969/j.issn.1673-5374.2012.23.009
    The lack of curative therapies for neurodegenerative diseases has high economic impact and places huge burden on the society. The contribution of stem cells to cure neurodegenerative diseases has been unraveled and explored extensively over the past few years. Beyond substitution of the lost neurons, stem cells act as immunomodulators and neuroprotectors. A large number of preclinical and a small number of clinical studies have shown beneficial outcomes in this context. In this review, we have summarized the current concepts of stem cell therapy in neurodegenerative diseases and the recent advances in this field, particularly between 2010 and 2012. Further studies should be encouraged to resolve the clinical issues and vague translational findings for maximum optimization of the efficacy of stem cell therapy in neurodegenerative diseases.
    Matched MeSH terms: Neurons
  6. Fulltext Neural Commitment of Embryonic Stem Cells through the Formation of Embryoid Bodies (EBs)
    Liyang G, Abdullah S, Rosli R, Nordin N
    Malays J Med Sci, 2014 Sep-Oct;21(5):8-16.
    PMID: 25977628 MyJurnal
    An embryonic stem cell (ESC) is a good tool to generate neurons in vitro and can be used to mimic neural development in vivo. It has been widely used in research to examine the role of cell signalling during neuronal development, test the effects of drugs on neurons, and generate a large population of functional neurons. So far, a number of protocols have been established to promote the differentiation of ESCs, such as direct and indirect differentiation. One of the widely used protocols to generate neurons is through the spontaneous formation of multicellular aggregates known as embryonic bodies (EBs). However, for some, it is not clear why EB protocol could be the protocol of choice. EB also is known to mimic an early embryo; hence, knowing the similarities between EB and an early embryo is essential, particularly the information on the players that promote the formation of EBs or the aggregation of ESCs. This review paper focuses on these issues and discusses further the generation of neural cells from EBs using a well-known protocol, the 4-/4+ protocol.
    Matched MeSH terms: Neurons
  7. Fulltext Induced mitochondrial membrane potential for modeling solitonic conduction of electrotonic signals
    Poznanski RR, Cacha LA, Ali J, Rizvi ZH, Yupapin P, Salleh SH, et al.
    PLoS One, 2017;12(9):e0183677.
    PMID: 28880876 DOI: 10.1371/journal.pone.0183677
    A cable model that includes polarization-induced capacitive current is derived for modeling the solitonic conduction of electrotonic potentials in neuronal branchlets with microstructure containing endoplasmic membranes. A solution of the nonlinear cable equation modified for fissured intracellular medium with a source term representing charge 'soakage' is used to show how intracellular capacitive effects of bound electrical charges within mitochondrial membranes can influence electrotonic signals expressed as solitary waves. The elastic collision resulting from a head-on collision of two solitary waves results in localized and non-dispersing electrical solitons created by the nonlinearity of the source term. It has been shown that solitons in neurons with mitochondrial membrane and quasi-electrostatic interactions of charges held by the microstructure (i.e., charge 'soakage') have a slower velocity of propagation compared with solitons in neurons with microstructure, but without endoplasmic membranes. When the equilibrium potential is a small deviation from rest, the nonohmic conductance acts as a leaky channel and the solitons are small compared when the equilibrium potential is large and the outer mitochondrial membrane acts as an amplifier, boosting the amplitude of the endogenously generated solitons. These findings demonstrate a functional role of quasi-electrostatic interactions of bound electrical charges held by microstructure for sustaining solitons with robust self-regulation in their amplitude through changes in the mitochondrial membrane equilibrium potential. The implication of our results indicate that a phenomenological description of ionic current can be successfully modeled with displacement current in Maxwell's equations as a conduction process involving quasi-electrostatic interactions without the inclusion of diffusive current. This is the first study in which solitonic conduction of electrotonic potentials are generated by polarization-induced capacitive current in microstructure and nonohmic mitochondrial membrane current.
    Matched MeSH terms: Neurons/physiology*
  8. Muscle spindles provide servo-assistance to jaw-closing muscles for chewing hard foods
    Zakir H, Fathilah A, Bakri M, Kitagawa J
    Sains Malaysiana, 2015;44:593-597.
    The fundamental pattern of chewing induced by the network of neurons called central pattern generator has been reported
    to be modified by the information arising from the various oro-facial sensory receptors including muscle spindles of jaw
    closing muscles. The cell bodies of primary afferent neurons from these muscle spindles lie in mesencephalic trigeminal
    nucleus (MTN) in the brainstem. The aim of the study was to understand whether muscle spindles from jaw-closing
    muscles play any role in hard food chewing. Single neuronal discharge of muscle spindle afferents was recorded from the
    MTN simultaneous with jaw-movement and electromyograpic (EMG) activities of the left masseter (jaw-closing) muscle
    during chewing soft and hard foods (apple and pellet) in awake rabbits. Ten consecutive chewing cycles were taken for
    analysis. Discharge of nineteen muscle spindles from seven rabbits was successfully recorded. Muscle-spindle discharge
    was significantly higher during the closing phase of jaw-movement for the hard food chewing than for the soft food. The
    jaw-closing muscle EMG activity was significantly higher during hard food chewing compared to soft food. The spindle
    discharge was higher when the masseter muscle activity was greater for chewing hard food. Significant positive (r=0.822,
    p=<0.001) correlation was found between the difference of muscle activity between apple and pellet and the difference
    of spindle discharge between apple and pellet. Above findings suggest that the increase of spindle discharge during
    hard food chewing may play a role for facilitating jaw-closing muscle activities and thereby provides servo-assistance
    to jaw-closing muscles to compensate the hardness of food.
    Matched MeSH terms: Neurons; Neurons, Afferent
  9. Unveiling the Role of Cytochrome P450 (2E1) in Human Brain Specifically in Parkinson's Disease - Literature Review
    Shah A, Ong CE, Pan Y
    Curr Drug Metab, 2021;22(9):698-708.
    PMID: 34325630 DOI: 10.2174/1389200222666210729115151
    BACKGROUND: In recent years, the significance of cytochrome P450 enzymes (CYPs) has expanded beyond their role in the liver. Factors such as genetics, environmental toxins, drug biotransformation and underlying diseases mediate the expression of these enzymes. Among the CYP enzymes, CYP2E1, a well-recognized monooxygenase enzyme involved in the metabolism of various endogenous and exogenous substances, plays a crucial role in the brain concerning the development of Parkinson's disease. The expression of CYP2E1 varies in different brain regions making certain regions more vulnerable than others. CYP2E1 expression is inducible which generates tissuedamaging radicals leading to oxidative stress, mitochondrial dysfunction and ultimately neurodegeneration.

    OBJECTIVE: Less is understood about the role of CYP2E1 in the central nervous system, therefore the purpose of the study was to investigate the relationship between the expression and activity of CYP2E1 enzyme relevant to Parkinson's disease and to identify whether an increase in the expression of CYP2E1 is associated with neurodegeneration.

    METHODS: The objectives of the study were achieved by implicating an unsystematic integrative literature review approach in which the literature was qualitatively analysed, critically evaluated and a new theory with an overall view of the mechanism was presented.

    RESULTS: The contribution of CYP2E1 in the development of Parkinson's disease was found to be significant as the negative effects of CYP2E1 overshadowed its protective detoxifying role.

    CONCLUSION: Overexpression of CYP2E1 seems detrimental to dopaminergic neurons, therefore, to overcome this, a synthetic biochemical is required, which paves the way for further research and development of valuable biomolecules.

    Matched MeSH terms: Dopaminergic Neurons/metabolism
  10. Fulltext Relationship between anthropometric and biochemical changes of metabolic syndrome with retinal nerve fiber layer and macular thickness
    New SH, Leow SN, Vasudevan SK, Idris IB, Tang SF, Din NM
    PLoS One, 2021;16(2):e0246830.
    PMID: 33630879 DOI: 10.1371/journal.pone.0246830
    OBJECTIVE: To evaluate the retinal nerve fiber layer (RNFL) and macular thicknesses and identify systemic risk factors for thinning of these layers in patients with metabolic syndrome (MetS).

    METHODOLOGY: A cross-sectional observational study was performed on patients diagnosed with MetS and compared to normal controls. All patients underwent ophthalmic and anthropometric examination, serological and biochemical blood investigations; and ocular imaging using spectral-domain optical coherence tomography. Patients with ocular pathology were excluded. Unpaired t-test was used to compare mean thickness between the two groups. One-way ANOVA with Bonferroni correction for multiple comparisons was used to compare mean thickness between different tertiles of MetS parameters, and a generalized estimating equation was used to correct for inter-eye correlation and to assess association between mean thickness and covariates.

    RESULTS: Two hundred and forty-eight eyes from 124 participants (1:1 ratio of MetS patients to controls) were included. Age ranged between 30 to 50 years old, and mean age was 40 ± 6.6 years. RNFL thickness was lower globally (93.6 ± 9.9 μm vs 99.0 ± 9.3, p<0.001) and in the inferior (124.5 ± 17.5 μm vs 131.0 ± 16.4 μm, p = 0.002), superior (117.2 ± 16.0 μm vs 126.3 ± 14.4 μm, p<0.001) and temporal (65.5 ± 10.2 μm vs 69.5 ± 9.8, p = 0.002) sectors in MetS patients compared to controls. Only the central (237.0 ± 14.0 μm vs 243.6 ± 18.0 μm, p = 0.002) and inferior parafoveal (307.8 ± 20.9 vs 314.6 ± 14.6, p = 0.004) area of the macula was significantly thinner. The inferior RNFL sector had the most difference (mean difference = 9.1 μm). The Generalized Estimating Equation found that, after adjusting for age, diastolic blood pressure, BMI, HDL and obesity; the number of MetS components and elevated triglyceride levels were independent risk factors for reduced thickness in global RNFL (β = -4.4, 95% CI = -7.29 to -1.5, p = 0.003) and inferior parafovea (β = -6.85, 95% CI = -11.58 to -2.13, p = 0.004) thickness respectively.

    CONCLUSION: RNFL thinning was seen more than macula thinning in MetS patients, suggesting RNFL susceptibility to neurodegeneration than the macula. A higher number of metabolic components and elevated triglyceride levels were independent risk factors for retinal thinning in this group of patients.

    Matched MeSH terms: Retinal Neurons/pathology*
  11. Functional Neuroproteomics: An Imperative Approach for Unravelling Protein Implicated Complexities of Brain
    Husain I, Ahmad W, Ali A, Anwar L, Nuruddin SM, Ashraf K, et al.
    CNS Neurol Disord Drug Targets, 2021;20(7):613-624.
    PMID: 33530918 DOI: 10.2174/1871527320666210202121624
    A proteome is defined as a comprehensive protein set either of an organ or an organism at a given time and under specific physiological conditions. Accordingly, the study of the nervous system's proteomes is called neuroproteomics. In the neuroproteomics process, various pieces of the nervous system are "fragmented" to understand the dynamics of each given sub-proteome in a much better way. Functional proteomics addresses the organisation of proteins into complexes and the formation of organelles from these multiprotein complexes that control various physiological processes. Current functional studies of neuroproteomics mainly talk about the synapse structure and its organisation, the major building site of the neuronal communication channel. The proteomes of synaptic vesicle, presynaptic terminal, and postsynaptic density, have been examined by various proteomics techniques. The objectives of functional neuroproteomics are: to solve the proteome of single neurons or astrocytes grown in cell cultures or from the primary brain cells isolated from tissues under various conditions, to identify the set of proteins that characterize specific pathogenesis, or to determine the group of proteins making up postsynaptic or presynaptic densities. It is usual to solve a particular sub-proteome like the heat-shock response proteome or the proteome responding to inflammation. Post-translational protein modifications alter their functions and interactions. The techniques to detect synapse phosphoproteome are available. However, techniques for the analysis of ubiquitination and sumoylation are under development.
    Matched MeSH terms: Neurons/physiology
  12. The potential role of miRNA therapies in spinal muscle atrophy
    Gandhi G, Abdullah S, Foead AI, Yeo WWY
    J Neurol Sci, 2021 08 15;427:117485.
    PMID: 34015517 DOI: 10.1016/j.jns.2021.117485
    Spinal muscular atrophy (SMA) is a neurodegenerative disease caused by low levels of full-length survival motor neuron (SMN) protein due to the loss of the survival motor neuron 1 (SMN1) gene and inefficient splicing of the survival motor neuron 2 (SMN2) gene, which mostly affects alpha motor neurons of the lower spinal cord. Despite the U.S. Food and Drug Administration (FDA) approved SMN-dependent therapies including Nusinersen, Zolgensma® and Evrysdi™, SMA is still a devastating disease as these existing expensive drugs may not be sufficient and thus, remains a need for additional therapies. The involvement of microRNAs (miRNAs) in SMA is expanding because miRNAs are important mediators of gene expression as each miRNA could target a number of genes. Hence, miRNA-based therapy could be utilized in treating this genetic disorder. However, the delivery of miRNAs into the target cells remains an obstacle in SMA, as there is no effective delivery system to date. This review highlights the potential strategies for intracellular miRNA delivery into target cells and current challenges in miRNA delivery. Furthermore, we provide the future prospects of miRNA-based therapeutic strategies in SMA.
    Matched MeSH terms: Motor Neurons/pathology
  13. RFamide peptides as mediators in environmental control of GnRH neurons
    Parhar I, Ogawa S, Kitahashi T
    Prog. Neurobiol., 2012 Aug;98(2):176-96.
    PMID: 22684005 DOI: 10.1016/j.pneurobio.2012.05.011
    Hypothalamic gonadotropin-releasing hormone (GnRH) is a key hormone for reproductive functions in vertebrates and non-vertebrates. Although GnRH neuronal system is regulated by several factors such as steroids, neurotransmitters and neuropeptides, it is not fully understood how environmental signals control the GnRH neuronal system. RFamide peptides, members of peptides possessing an Arg-Phe-NH(2) motif at their C-terminus, have recently been characterized as major regulators of GnRH neurons. In particular, two key RFamide peptides, kisspeptin and gonadotropin-inhibitory hormone (GnIH), are emerging as important regulators of the reproductive axis. Kisspeptin acts as the accelerator, directly driving GnRH neurons, whereas GnIH acts as the restraint. In addition, other RFamide peptides such as prolactin-releasing peptide (PrRP), PQRFa peptide, 26RFa/QRFP are also known to control reproduction. These RFamide peptides are regulated by environmental factors such as photoperiods, steroid hormones, metabolic signals, and stress. How environmental signals are integrated by RFamide peptides to regulate reproduction through the GnRH neurons?
    Matched MeSH terms: Neurons/metabolism*
  14. Alpha terpineol directs bone marrow mesenchymal stem cells toward neuronal lineage through regulation of wnt signaling pathway
    Ishaque A, Salim A, Simjee SU, Khan I, Adli DSH
    Cell Biochem Funct, 2023 Mar;41(2):223-233.
    PMID: 36651266 DOI: 10.1002/cbf.3775
    Central nervous system anomalies give rise to neuropathological consequences with immense damage to the neuronal tissues. Cell based therapeutics have the potential to manage several neuropathologies whereby the differentiated cells are explored for neuronal regeneration. The current study analyzes the effect of a bioactive compound, alpha terpineol (AT) on the differentiation of rat bone marrow derived mesenchymal stem cells (BM-MSCs) toward neuronal lineage, and explores regulation of differentiation process through the study of Wnt pathway mediators. BM-MSCs were cultured and characterized based on their surface markers and tri-lineage differentiation. Safe dose of AT as optimized by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium bromide assay, was used for the treatment of MSCs. Treated cells were analyzed for the neuronal, astroglial and germ layer transition markers at the gene and protein levels, by quantitative polymerase chain reaction and immunocytochemistry, respectively. Temporal expression of Wnt pathway genes was assessed during the course of neuronal differentiation. AT treated group showed significant upregulation of neuron specific (NSE, MAP2, Tau, Nestin, and NefL) and astroglial (GFAP) genes with positive expression of late neuronal markers. Germ layer transition analysis showed the overexpression of ectodermal markers (NCAM, Nestin, and Pax6), whereas endodermal (AFP, MixL1, and Sox17), and mesodermal (Mesp1 and T Brachyury) markers were also found to be upregulated. Wnt signaling pathway was activated during the initial phase (30 min) of differentiation, which later was downregulated at 1, 3, and 5 h. AT efficiently induces neuronal differentiation of BM-MSCs by regulating Wnt signaling. Overexpression of both early and late neuronal markers indicate their neuro-progenitor state and thus can be utilized as a promising approach in cellular therapeutics to treat various neurodegenerative ailments. In addition, exploration of the molecular pathways may be helpful to understand the mechanism of cell-based neuronal regeneration.
    Matched MeSH terms: Neurons/metabolism
  15. Fulltext MDGA2 homozygous loss-of-function variants cause developmental and epileptic encephalopathy
    Morsy H, Kim H, Jang G, Zaki MS, Severino M, Abdelrazek IM, et al.
    Am J Hum Genet, 2026 Feb 05;113(2):380-391.
    PMID: 41570816 DOI: 10.1016/j.ajhg.2025.12.015
    MDGA2 encodes a membrane-associated protein that is critical for regulating glutamatergic synapse development, modulating neuroligins (Nlgns), and maintaining excitatory-inhibitory synaptic balance. While MDGA2 functions have been extensively studied in murine and cellular models, its association with human developmental disorders has yet to be established. Through exome sequencing, we identified seven distinct homozygous loss-of-function variants in MDGA2 in nine individuals from seven consanguineous families, all presenting with developmental and epileptic encephalopathy (DEE). Clinically, these individuals exhibited a consistent phenotype including infantile hypotonia, severe neurodevelopmental delay, intractable seizures, along with distinct dysmorphic features. Neuroimaging findings included delayed/incomplete myelination, early-onset brain atrophy, white-matter thinning, basal ganglia volume loss, and small hippocampi. Functional studies of three representative nonsense variants revealed impaired MDGA2 membrane trafficking, disrupted Nlgn1 interaction, and perturbed MDGA2-mediated excitatory synaptic functions in mammalian expression systems and cultured hippocampal neurons. Our findings support the involvement of MDGA2 in a subtype of autosomal-recessive DEE. This not only underscores a loss-of-function pathogenic mechanism but also highlights the previously unrecognized role of MDGA2 in human synaptic development and regulation, significantly expanding our understanding of the genetic architecture of DEEs.
    Matched MeSH terms: Neurons/metabolism
  16. Fulltext RSAD2 and AIM2 Modulate Coxsackievirus A16 and Enterovirus A71 Replication in Neuronal Cells in Different Ways That May Be Associated with Their 5' Nontranslated Regions
    Yogarajah T, Ong KC, Perera D, Wong KT
    J Virol, 2018 03 15;92(6).
    PMID: 29263272 DOI: 10.1128/JVI.01914-17
    Coxsackievirus A16 (CV-A16) and enterovirus A71 (EV-A71) are closely related enteroviruses that cause the same hand, foot, and mouth disease (HFMD), but neurological complications occur only very rarely in CV-A16 compared to EV-A71 infections. To elucidate host responses that may be able to explain these differences, we performed transcriptomic analysis and real-time quantitative PCR (RT-qPCR) in CV-A16-infected neuroblastoma cells (SK-N-SH), and the results showed that the radical S-adenosylmethionine domain containing 2 (RSAD2) was the highest upregulated gene in the antimicrobial pathway. Increased RSAD2 expression was correlated with reduced viral replication, while RSAD2 knockdown cells were correlated with increased replication. EV-A71 replication showed no apparent correlation to RSAD2 expressions. Absent in melanoma 2 (AIM2), which is associated with pyroptotic cell death, was upregulated in EV-A71-infected neurons but not in CV-A16 infection, suggesting that the AIM2 inflammasome played a significant role in suppressing EV-A71 replication. Chimeric viruses derived from CV-A16 and EV-A71 but containing swapped 5' nontranslated regions (5' NTRs) showed that RSAD2 expression/viral replication and AIM2 expression/viral replication patterns may be linked to the 5' NTRs of parental viruses. Differences in secondary structure of internal ribosomal entry sites within the 5' NTR may be responsible for these findings. Overall, our results suggest that CV-A16 and EV-A71 elicit different host responses to infection, which may help explain the apparent lower incidence of CV-A16-associated neurovirulence in HFMD outbreaks compared to EV-A71 infection.IMPORTANCE Although coxsackievirus A16 (CV-A16) and enterovirus A17 (EV-A71) both cause hand, foot, and mouth disease, EV-A71 has emerged as a leading cause of nonpolio, enteroviral fatal encephalomyelitis among young children. The significance of our research is in the identification of the possible differing and novel mechanisms of CV-A16 and EV-A71 inhibition in neuronal cells that may impact viral neuropathogenesis. We further showed that viral 5' NTRs may play significant roles in eliciting different host response mechanisms.
    Matched MeSH terms: Neurons/metabolism*; Neurons/pathology; Neurons/virology
  17. Harnessing neuroplasticity: modern approaches and clinical future
    Sasmita AO, Kuruvilla J, Ling APK
    Int J Neurosci, 2018 Nov;128(11):1061-1077.
    PMID: 29667473 DOI: 10.1080/00207454.2018.1466781
    Background and purpose: Neurological diseases and injuries to the nervous system may cause inadvertent damage to neuronal and synaptic structures. Such phenomenon would lead to the development of neurological and neurodegenerative disorders which might affect memory, cognition and motoric functions. The body has various negative feedback systems which can induce beneficial neuroplastic changes in mediating some neuronal damage; however, such efforts are often not enough to ameliorate the derogatory changes. Materials and methods: Articles discussing studies to induce beneficial neuroplastic changes were retrieved from the databases, National Center for Biotechnology Information (NCBI) and MEDLINE, and reviewed. Results: This review highlights the significance of neuroplasticity in restoring neuronal functions and current advances in research to employ this positive cellular event by inducing synaptogenesis, neurogenesis, clearance of toxic amyloid beta (Aβ) and tau protein aggregates, or by providing neuroprotection. Compounds ranging from natural products (e.g. bilobalides, curcumin) to novel vaccines (e.g. AADvac1, RG7345) have been reported to induce long-lasting neuroplasticity in vitro and in vitro. Activity-dependent neuroplasticity is also inducible by regimens of exercises and therapies with instances in human studies proving major successes. Lastly, mechanical stimulation of brain regions through therapeutic hypothermia or deep brain stimulation has given insight on the larger scale of neuroplasticity within the nervous system. Conclusion: Harnessing neuroplasticity may not only offer an arm in the vast arsenal of approaches being taken to tackle neurological disorders, such as neurodegenerative diseases, but from ample evidence, it also has major implications in neuropsychological disorders.
    Matched MeSH terms: Neurons/drug effects; Neurons/metabolism*; Neurons/pathology
  18. Fulltext Kisspeptin-1 regulates forebrain dopaminergic neurons in the zebrafish
    Abdul Satar NM, Ogawa S, Parhar IS
    Sci Rep, 2020 11 09;10(1):19361.
    PMID: 33168887 DOI: 10.1038/s41598-020-75777-0
    The habenula is a phylogenetically conserved epithalamic structure, which conveys negative information via inhibition of mesolimbic dopamine neurons. We have previously shown the expression of kisspeptin (Kiss1) in the habenula and its role in the modulation of fear responses in the zebrafish. In this study, to investigate whether habenular Kiss1 regulates fear responses via dopamine neurons in the zebrafish, Kiss1 peptides were intracranially administered close to the habenula, and the expression of dopamine-related genes (th1, th2 and dat) were examined in the brain using real-time PCR and dopamine levels using LC-MS/MS. th1 mRNA levels and dopamine levels were significantly increased in the telencephalon 24-h and 30-min after Kiss1 administration, respectively. In fish administered with Kiss1, expression of neural activity marker gene, npas4a and kiss1 gene were significantly decreased in the ventral habenula. Application of neural tracer into the median raphe, site of habenular Kiss1 neural terminal projections showed tracer-labelled projections in the medial forebrain bundle towards the telencephalon where dopamine neurons reside. These results suggest that Kiss1 negatively regulates its own neuronal activity in the ventral habenula via autocrine action. This, in turn affects neurons of the median raphe via interneurons, which project to the telencephalic dopaminergic neurons.
    Matched MeSH terms: Interneurons/metabolism; Neurons/metabolism; Dopaminergic Neurons/metabolism*
  19. Fulltext Spinal muscular atrophy
    Sasongko, Teguh Haryo, Zilfalil Alwi
    Buletin Persatuan Genetik Malaysia, 2009;14(1):8-13.
    MyJurnal
    Spinal muscular atrophy (SMA), a leading genetic cause of death in childhood, is caused by deletion of the SMN1 gene, located at chromosome 5q13. The molecular pathogenesis, which results in motor neuron degeneration within the anterior horn of spinal cord, is a focus of debate among scientists. The unique nature of the duplicative 5q chromosomal region provides considerable yet challenging opportunity for disease correction as well as complication in performing molecular diagnosis and understanding the molecular pathogenesis. This article reviewed recent findings in the molecular pathogenesis of SMA as well as the research advances in the molecular diagnosis and therapeutic approaches.
    Matched MeSH terms: Motor Neurons
  20. Fulltext Pengaktifan otak akibat gerakan jari bagi subjek dominan tangan kanan dan kiri
    Ahmad Nazlim Yusoff, Mohd Harith Hashim, Mohd Mahadir Ayob, Iskandar Kassim
    Jurnal Sains Kesihatan Malaysia, 2006;4(2):63-83.
    MyJurnal
    Kajian garis pangkal pengimejan resonans magnet kefungsian (fMRI) telah dijalankan ke atas 2 orang subjek lelaki sihat dominan tangan kanan dan kiri. Kajian ini menggunakan gerakan jari tangan kanan dan kiri untuk merangsang aktiviti neuron di dalam korteks serebrum. Subjek diarahkan supaya menekan jari-jari pada ibu jari secara bergilir-gilir semasa imbasan fMRI dilakukan. Paradigma 5 kitar aktif-rehat digunakan dengan setiap kitar mengandungi satu blok aktif dan satu blok rehat dengan 10 siri pengukuran untuk setiap blok. Seratus isipadu imej fMRI bagi setiap subjek dianalisis menggunakan pekej perisian MatLab dan SPM2. Model linear am (GLM) digunakan untuk menganggar secara statistik parameter yang mencirikan model rangsangan hemodinamik bagi gerakan jari. Kesimpulan mengenai pengaktifan otak yang diperhatikan dijana secara statistik berasaskan teori medan rawak (RFT) Gaussian. Keputusan menunjukkan bahawa rantau otak yang aktif akibat gerakan jari adalah pada girus presentral merangkumi kawasan motor primer. Pengaktifan otak adalah secara kontralateral terhadap gerakan jari tangan kanan dan kiri. Keamatan isyarat keadaan aktif didapati lebih tinggi secara bererti (p < 0.001) daripada keamatan isyarat keadaan rehat. Bilangan voksel yang aktif didapati lebih tinggi pada hemisfera otak yang mengawal gerakan jari bagi tangan yang tidak dominan untuk kedua-dua subjek. Keputusan ini menyokong fakta bahawa kawasan pengaktifan motor pada hemisfera otak semasa gerakan jari tangan yang tidak dominan mengalami rangsangan hemodinamik yang lebih tinggi dan kawasan pengaktifan yang lebih luas berbanding dengan kawasan pengaktifan pada hemisfera otak yang mengawal gerakan jari bagi tangan yang dominan.
    Matched MeSH terms: Neurons
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