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  1 / 13990 MEDLINE  
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[PMID]:27777102
[Au] Autor:Mumaw CL; Surace M; Levesque S; Kodavanti UP; Kodavanti PRS; Royland JE; Block ML
[Ad] Endereço:Department of Anatomy and Cell Biology, The Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
[Ti] Título:Atypical microglial response to biodiesel exhaust in healthy and hypertensive rats.
[So] Source:Neurotoxicology;59:155-163, 2017 03.
[Is] ISSN:1872-9711
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence suggests a deleterious role for urban air pollution in central nervous system (CNS) diseases and neurodevelopmental disorders. Microglia, the resident innate immune cells and sentinels in the brain, are a common source of neuroinflammation and are implicated in air pollution-induced CNS effects. While renewable energy, such as soy-based biofuel, is of increasing public interest, there is little information on how soy biofuel may affect the brain, especially in people with preexisting disease conditions. To address this, male spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats were exposed to 100% Soy-based Biodiesel Exhaust (100SBDE; 0, 50, 150 and 500µg/m ) by inhalation, 4h/day for 4 weeks (5 days/week). Ionized calcium-binding adapter molecule-1 (IBA-1) staining of microglia in the substantia nigra revealed significant changes in morphology with 100SBDE exposure in rats from both genotypes, where SHR were less sensitive. Aconitase activity was inhibited in the frontal cortex and cerebellum of WKY rats exposed to 100SBDE. No consistent changes occurred in pro-inflammatory cytokine expression, nitrated protein, or arginase1 expression in brain regions from either rat strain exposed to 100SBDE. However, while IBA-1 mRNA expression was not modified, CX3CR1 mRNA expression was lower in the striatum of 100SBDE exposed rats regardless of genotype, suggesting a downregulation of the fractalkine receptor on microglia in this brain region. Together, these data indicate that while microglia are detecting and responding to 100SBDE exposure with changes in morphology, there is reduced expression of CX3CR1 regardless of genetic background and the activation response is atypical without traditional inflammatory markers of M1 or M2 activation in the brain.
[Mh] Termos MeSH primário: Biocombustíveis/toxicidade
Quimiocina CX3CL1/metabolismo
Hipertensão/fisiopatologia
Microglia/efeitos dos fármacos
Substância Negra/patologia
Emissões de Veículos/toxicidade
[Mh] Termos MeSH secundário: Aconitato Hidratase/metabolismo
Animais
Antioxidantes/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Citocinas/metabolismo
Relação Dose-Resposta a Droga
Hipertensão/genética
Hipertensão/patologia
Masculino
Proteínas dos Microfilamentos/metabolismo
Microglia/classificação
Estresse Oxidativo/efeitos dos fármacos
RNA Mensageiro/metabolismo
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Tirosina/análogos & derivados
Tirosina/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Antioxidants); 0 (Biofuels); 0 (Calcium-Binding Proteins); 0 (Chemokine CX3CL1); 0 (Cytokines); 0 (Microfilament Proteins); 0 (RNA, Messenger); 0 (Vehicle Emissions); 3604-79-3 (3-nitrotyrosine); 42HK56048U (Tyrosine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 4.2.1.3 (Aconitate Hydratase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  2 / 13990 MEDLINE  
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[PMID]:29244466
[Au] Autor:Timofeeva MR; Lukina SA
[Ti] Título:Surfactant system and water balance of the lungs in modeling of neurodegeneration and focus of pathological activity in the substantia nigra.
[So] Source:Patol Fiziol Eksp Ter;60(3):31-5, 2016 Jul-Sep.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The comparative analysis of surfactant metabolism and water balance of the lungs in modeling the formation and neurodegeneration focus of pathological activity in the substantia nigra of the brain. Methods: Experiments were performed on male rats - nonlinear, including the control, sham operated with unilateral stereotaxic administration of the neurotoxin 6-hydroxydopamine (Sigma) in the substantia nigra compact part and the implantation of cobalt metal nanopowder (Berlin) in the reticular part of the structure. Complex investigations included determination of surfactant phospholipid fractions by thin layer chromatography, total phospholipids and cholesterol in the bronchoalveolar lavage and surface-active properties by the Wilhelmy method, phospholipase activity, lipid peroxidation intensity on the content of TBA-active products in the lung tissue, evaluation of water balance using the gravimetric method. Results: It has been established that the introduction of intranigral neurotoxin and implantation of cobalt in the structure of the brain called the deterioration of the surface activity of the alveolar lining set against the backdrop of an imbalance of fractional composition of surfactant lipids with multidirectional changes in the amount of phospholipids and the degree of hydration of the lung. Induction focus of pathological activity in the substantia nigra was accompanied by an increase in alveolar phospholipids by lysophosphatidylcholine, sphingomyelin, phosphatidylethanolamine, intensification of lipid peroxidation of the lung tissue and organ hyperhydration. Modeling neurodegeneration - reduction of total phospholipids, phosphatidylcholine and lysophosphatidylcholine accumulation in terms of activation of phospholipase hydrolysis, increasing blood supply to the lungs. Conclusion: Metabolism of surfactant lipids and water balance in the lung, along with changes of rhythmogenesis and mode of ventilation, may lead to the development of disregulation of pneumopathy with dysfunction of the substantia nigra of the brain.
[Mh] Termos MeSH primário: Pulmão/metabolismo
Doenças Neurodegenerativas/metabolismo
Surfactantes Pulmonares/metabolismo
Substância Negra/metabolismo
Equilíbrio Hidroeletrolítico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Pulmão/patologia
Masculino
Doenças Neurodegenerativas/patologia
Ratos
Substância Negra/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pulmonary Surfactants)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


  3 / 13990 MEDLINE  
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[PMID]:29243900
[Au] Autor:Tarasova TV; Ustyugov AA; Ninkina NN; Skvortsova VI
[Ti] Título:The new line of genetically modified mice with constitutive knockout of the gene alpha synuclein to study pathogenetic aspects of differential loss of dopaminergic neurons .
[So] Source:Patol Fiziol Eksp Ter;60(3):4-9, 2016 Jul-Sep.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The purpose: This study investigated the role of alpha-synuclein in the development of dopaminergic neurons. Methods: In this study a new SNCA knockout mouse line has been used to model the deficiency of alpha-synuclein function. In the knockout and control mice the dynamics of the formation of two distinct populations of dopaminergic neurons differently affected in patients with PD was studied by the comparative morphometric analysis. Results: Here, we revealed a prominent modulating effect of alpha-synuclein on the developing DA neurons in substantia nigra (SN) which is the most affected region in PD patients. Yet, alpha-synuclein had no effect on the formation of DA neurons in ventral tegmental area which is much less susceptible to degeneration in PD patients. Conclusion: The new line of knockout mice is a convenient model for studying pathophysiologic aspects of selective impairment of DA neurons.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/metabolismo
Doença de Parkinson
Substância Negra
Área Tegmentar Ventral
alfa-Sinucleína/genética
[Mh] Termos MeSH secundário: Animais
Neurônios Dopaminérgicos/patologia
Camundongos
Camundongos Knockout
Doença de Parkinson/genética
Doença de Parkinson/metabolismo
Doença de Parkinson/patologia
Doença de Parkinson/fisiopatologia
Substância Negra/metabolismo
Substância Negra/patologia
Substância Negra/fisiopatologia
Área Tegmentar Ventral/metabolismo
Área Tegmentar Ventral/patologia
Área Tegmentar Ventral/fisiopatologia
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Snca protein, mouse); 0 (alpha-Synuclein)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


  4 / 13990 MEDLINE  
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[PMID]:29244806
[Au] Autor:Hammond SL; Leek AN; Richman EH; Tjalkens RB
[Ad] Endereço:Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO, United States of America.
[Ti] Título:Cellular selectivity of AAV serotypes for gene delivery in neurons and astrocytes by neonatal intracerebroventricular injection.
[So] Source:PLoS One;12(12):e0188830, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The non-pathogenic parvovirus, adeno-associated virus (AAV), is an efficient vector for transgene expression in vivo and shows promise for treatment of brain disorders in clinical trials. Currently, there are more than 100 AAV serotypes identified that differ in the binding capacity of capsid proteins to specific cell surface receptors that can transduce different cell types and brain regions in the CNS. In the current study, multiple AAV serotypes expressing a GFP reporter (AAV1, AAV2/1, AAVDJ, AAV8, AAVDJ8, AAV9, AAVDJ9) were screened for their infectivity in both primary murine astrocyte and neuronal cell cultures. AAV2/1, AAVDJ8 and AAV9 were selected for further investigation of their tropism throughout different brain regions and cell types. Each AAV was administered to P0-neonatal mice via intracerebroventricular injections (ICV). Brains were then systematically analyzed for GFP expression at 3 or 6 weeks post-infection in various regions, including the olfactory bulb, striatum, cortex, hippocampus, substantia nigra (SN) and cerebellum. Cell counting data revealed that AAV2/1 infections were more prevalent in the cortical layers but penetrated to the midbrain less than AAVDJ8 and AAV9. Additionally, there were differences in the persistence of viral transgene expression amongst the three serotypes examined in vivo at 3 and 6 weeks post-infection. Because AAV-mediated transgene expression is of interest in neurodegenerative diseases such as Parkinson's Disease, we examined the SN with microscopy techniques, such as CLARITY tissue transmutation, to identify AAV serotypes that resulted in optimal transgene expression in either astrocytes or dopaminergic neurons. AAVDJ8 displayed more tropism in astrocytes compared to AAV9 in the SN region. We conclude that ICV injection results in lasting expression of virally encoded transgene when using AAV vectors and that specific AAV serotypes are required to selectively deliver transgenes of interest to different brain regions in both astrocytes and neurons.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Dependovirus/genética
Terapia Genética/métodos
Neurônios/metabolismo
Substância Negra/metabolismo
Transgenes
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Astrócitos/citologia
Cerebelo/citologia
Cerebelo/metabolismo
Córtex Cerebral/citologia
Córtex Cerebral/metabolismo
Corpo Estriado/citologia
Corpo Estriado/metabolismo
Dependovirus/classificação
Dependovirus/metabolismo
Expressão Gênica
Genes Reporter
Vetores Genéticos
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Hipocampo/citologia
Hipocampo/metabolismo
Injeções Intraventriculares
Camundongos
Neurônios/citologia
Bulbo Olfatório/citologia
Bulbo Olfatório/metabolismo
Imagem Óptica
Especificidade de Órgãos
Cultura Primária de Células
Sorogrupo
Substância Negra/citologia
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188830


  5 / 13990 MEDLINE  
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[PMID]:29176896
[Au] Autor:Arnold JC; Cantu MA; Kasanga EA; Nejtek VA; Papa EV; Bugnariu N; Salvatore MF
[Ad] Endereço:Department of Pharmacology, Toxicology, and Neuroscience, Louisiana State University Health Sciences Center, Shreveport, Louisiana, United States of America.
[Ti] Título:Aging-related limit of exercise efficacy on motor decline.
[So] Source:PLoS One;12(11):e0188538, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Identifying lifestyle strategies and allied neurobiological mechanisms that reduce aging-related motor impairment is imperative, given the accelerating number of retirees and increased life expectancy. A physically active lifestyle prior to old age can reduce risk of debilitating motor decline. However, if exercise is initiated after motor decline has begun in the lifespan, it is unknown if aging itself may impose a limit on exercise efficacy to decelerate further aging-related motor decline. In Brown-Norway/Fischer 344 F1 hybrid (BNF) rats, locomotor activity begins to decrease in middle age (12-18 months). One mechanism of aging-related motor decline may be decreased expression of GDNF family receptor, GFRα-1, which is decreased in substantia nigra (SN) between 12 and 30 months old. Moderate exercise, beginning at 18 months old, increases nigral GFRα-1 and tyrosine hydroxylase (TH) expression within 2 months. In aged rats, replenishing aging-related loss of GFRα-1 in SN increases TH in SN alone and locomotor activity. A moderate exercise regimen was initiated in sedentary male BNF rats in a longitudinal study to evaluate if exercise could attenuate aging-related motor decline when initiated at two different ages in the latter half of the lifespan (18 or 24 months old). Motor decline was reversed in the 18-, but not 24-month-old, cohort. However, exercise efficacy in the 18-month-old group was reduced as the rats reached 27 months old. GFRα-1 expression was not increased in either cohort. These studies suggest exercise can decelerate motor decline when begun in the latter half of the lifespan, but its efficacy may be limited by age of initiation. Decreased plasticity of GFRα-1 expression following exercise may limit its efficacy to reverse motor decline.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Atividade Motora
Condicionamento Físico Animal
[Mh] Termos MeSH secundário: Animais
Peso Corporal
Dopamina/metabolismo
Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Masculino
Ratos
Ratos Endogâmicos F344
Substância Negra/enzimologia
Substância Negra/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Cell Line-Derived Neurotrophic Factor Receptors); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188538


  6 / 13990 MEDLINE  
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[PMID]:29176874
[Au] Autor:Reyes-Corona D; Vázquez-Hernández N; Escobedo L; Orozco-Barrios CE; Ayala-Davila J; Moreno MG; Amaro-Lara ME; Flores-Martinez YM; Espadas-Alvarez AJ; Fernandez-Parrilla MA; Gonzalez-Barrios JA; Gutierrez-Castillo ME; González-Burgos I; Martinez-Fong D
[Ad] Endereço:Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados, Ciudad de México, México.
[Ti] Título:Neurturin overexpression in dopaminergic neurons induces presynaptic and postsynaptic structural changes in rats with chronic 6-hydroxydopamine lesion.
[So] Source:PLoS One;12(11):e0188239, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The structural effect of neurturin (NRTN) on the nigrostriatal dopaminergic system in animals remains unknown, although NRTN has been shown to be effective in Parkinson's disease animal models. Herein, we aimed to demonstrate that NRTN overexpression in dopaminergic neurons stimulates both neurite outgrowths in the nigrostriatal pathway and striatal dendritic spines in aging rats with chronic 6-hydroxydopamine (6-OHDA) lesion. At week 12 after lesion, pTracer-mNRTN-His or pGreenLantern-1 plasmids were intranigrally transfected using the NTS-polyplex nanoparticles system. We showed that the transgenic expression in dopaminergic neurons remained until the end of the study (12 weeks). Only animals expressing NRTN-His showed recovery of tyrosine hydroxylase (TH)+ cells (28 ± 2%), their neurites (32 ± 2%) and the neuron-specific cytoskeletal marker ß-III-tubulin in the substantia nigra; striatal TH(+) fibers were also recovered (52 ± 3%), when compared to the healthy condition. Neurotensin receptor type 1 levels were also significantly recovered in the substantia nigra and striatum. Dopamine recovery was 70 ± 4% in the striatum and complete in the substantia nigra. The number of dendritic spines of striatal medium spiny neurons was also significantly increased, but the recovery was not complete. Drug-activated circling behavior decreased by 73 ± 2% (methamphetamine) and 89 ± 1% (apomorphine). Similar decrease was observed in the spontaneous motor behavior. Our results demonstrate that NRTN causes presynaptic and postsynaptic restoration of the nigrostriatal dopaminergic system after a 6-OHDA-induced chronic lesion. However, those improvements did not reach the healthy condition, suggesting that NRTN exerts lesser neurotrophic effects than other neurotrophic approaches.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/metabolismo
Neurturina/metabolismo
Terminações Pré-Sinápticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Corpo Estriado/metabolismo
Corpo Estriado/patologia
Citoesqueleto/metabolismo
Espinhas Dendríticas/metabolismo
Dopamina/metabolismo
Ensaio de Imunoadsorção Enzimática
Membro Anterior/fisiologia
Masculino
Camundongos
Neuritos/metabolismo
Oxidopamina
Ratos Wistar
Receptores de Neurotensina/metabolismo
Substância Negra/metabolismo
Substância Negra/patologia
Transfecção
Vibrissas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurturin); 0 (Receptors, Neurotensin); 0 (neurotensin type 1 receptor); 8HW4YBZ748 (Oxidopamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188239


  7 / 13990 MEDLINE  
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[PMID]:29050386
[Au] Autor:Tong J; Rathitharan G; Meyer JH; Furukawa Y; Ang LC; Boileau I; Guttman M; Hornykiewicz O; Kish SJ
[Ad] Endereço:Preclinical Imaging Unit, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.
[Ti] Título:Brain monoamine oxidase B and A in human parkinsonian dopamine deficiency disorders.
[So] Source:Brain;140(9):2460-2474, 2017 Sep 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:See Jellinger (doi:10.1093/awx190) for a scientific commentary on this article. The enzyme monoamine oxidases (B and A subtypes, encoded by MAOB and MAOA, respectively) are drug targets in the treatment of Parkinson's disease. Inhibitors of MAOB are used clinically in Parkinson's disease for symptomatic purposes whereas the potential disease-modifying effect of monoamine oxidase inhibitors is debated. As astroglial cells express high levels of MAOB, the enzyme has been proposed as a brain imaging marker of astrogliosis, a cellular process possibly involved in Parkinson's disease pathogenesis as elevation of MAOB in astrocytes might be harmful. Since brain monoamine oxidase status in Parkinson's disease is uncertain, our objective was to measure, by quantitative immunoblotting in autopsied brain homogenates, protein levels of both monoamine oxidases in three different degenerative parkinsonian disorders: Parkinson's disease (n = 11), multiple system atrophy (n = 11), and progressive supranuclear palsy (n = 16) and in matched controls (n = 16). We hypothesized that if MAOB is 'substantially' localized to astroglial cells, MAOB levels should be generally associated with standard astroglial protein measures (e.g. glial fibrillary acidic protein). MAOB levels were increased in degenerating putamen (+83%) and substantia nigra (+10%, non-significant) in multiple system atrophy; in caudate (+26%), putamen (+27%), frontal cortex (+31%) and substantia nigra (+23%) of progressive supranuclear palsy; and in frontal cortex (+33%), but not in substantia nigra of Parkinson's disease, a region we previously reported no increase in astrocyte protein markers. Although the magnitude of MAOB increase was less than those of standard astrocytic markers, significant positive correlations were observed amongst the astrocyte proteins and MAOB. Despite suggestions that MAOA (versus MAOB) is primarily responsible for metabolism of dopamine in dopamine neurons, there was no loss of the enzyme in the parkinsonian substantia nigra; instead, increased nigral levels of a MAOA fragment and 'turnover' of the enzyme were observed in the conditions. Our findings provide support that MAOB might serve as a biochemical imaging marker, albeit not entirely specific, for astrocyte activation in human brain. The observation that MAOB protein concentration is generally increased in degenerating brain areas in multiple system atrophy (especially putamen) and in progressive supranuclear palsy, but not in the nigra in Parkinson's disease, also distinguishes astrocyte behaviour in Parkinson's disease from that in the two 'Parkinson-plus' conditions. The question remains whether suppression of either MAOB in astrocytes or MAOA in dopamine neurons might influence progression of the parkinsonian disorders.
[Mh] Termos MeSH primário: Encéfalo/enzimologia
Dopamina/deficiência
Monoaminoxidase/metabolismo
Atrofia de Múltiplos Sistemas/metabolismo
Doença de Parkinson/metabolismo
Paralisia Supranuclear Progressiva/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Núcleo Caudado/metabolismo
Feminino
Lobo Frontal/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Isoenzimas/metabolismo
Masculino
Meia-Idade
Atrofia de Múltiplos Sistemas/patologia
Degeneração Neural/patologia
Doença de Parkinson/patologia
Fragmentos de Peptídeos/metabolismo
Fosfopiruvato Hidratase/metabolismo
Putamen/metabolismo
Substância Negra/metabolismo
Paralisia Supranuclear Progressiva/patologia
Tubulina (Proteína)/metabolismo
Adulto Jovem
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 0 (Isoenzymes); 0 (Peptide Fragments); 0 (Tubulin); 0 (alpha-Synuclein); EC 1.4.3.4 (Monoamine Oxidase); EC 4.2.1.11 (Phosphopyruvate Hydratase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx172


  8 / 13990 MEDLINE  
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[PMID]:29016618
[Au] Autor:Gramsch C; Reuter I; Kraff O; Quick HH; Tanislav C; Roessler F; Deuschl C; Forsting M; Schlamann M
[Ad] Endereço:Department of Neuroradiology, University Hospital Giessen, Giessen, Germany.
[Ti] Título:Nigrosome 1 visibility at susceptibility weighted 7T MRI-A dependable diagnostic marker for Parkinson's disease or merely an inconsistent, age-dependent imaging finding?
[So] Source:PLoS One;12(10):e0185489, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Visualisation of nigrosome 1, a substructure of the healthy substantia nigra, was restricted in susceptibility weighted MR imaging in almost all patients with Parkinson's disease studied so far. The purpose of this study was to determine the degree of visibility of this substructure in subjects without Parkinson's disease and to examine the potential link between increasing brain iron accumulation with age and its detectability. METHODS: In 46 subjects (21 women, 25 men; 19 to 75 y; mean age: 44.5; SD: 15.6) examined with susceptibility weighted MR imaging at 7T visibility of nigrosome 1 was rated and classified. We assessed differences related to age and to signal intensities in the substantia nigra, red nucleus and putamen as correlates of the individual iron concentration. RESULTS: In 93% nigrosome 1was at least unilaterally clearly present. In 24% at least one-sided limited visibility was observed. Using predefined classification criteria the specificity of the visibility across all age groups reached approximately 94%. We found no correlation with increasing iron concentrations with age. CONCLUSION: Aging with a related increase in iron concentration probably does not affect the visibility of nigrosome 1 at 7T SWI MRI. Our results support the role of this feature as a future differential diagnostic tool but further large-scale prospective studies are needed to better define the extent of a "limited visibility" to which an individual can be considered healthy.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Imagem por Ressonância Magnética/métodos
Doença de Parkinson/diagnóstico por imagem
Substância Negra/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Envelhecimento/patologia
Mapeamento Encefálico/métodos
Feminino
Seres Humanos
Ferro/isolamento & purificação
Ferro/metabolismo
Masculino
Meia-Idade
Doença de Parkinson/metabolismo
Doença de Parkinson/patologia
Substância Negra/metabolismo
Substância Negra/patologia
Substância Negra/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
E1UOL152H7 (Iron)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185489


  9 / 13990 MEDLINE  
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[PMID]:28969384
[Au] Autor:Migdalska-Richards A; Wegrzynowicz M; Rusconi R; Deangeli G; Di Monte DA; Spillantini MG; Schapira AHV
[Ad] Endereço:Department of Clinical Neurosciences, Institute of Neurology, University College London, London NW3 2PF, UK.
[Ti] Título:The L444P Gba1 mutation enhances alpha-synuclein induced loss of nigral dopaminergic neurons in mice.
[So] Source:Brain;140(10):2706-2721, 2017 Oct 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mutations in glucocerebrosidase 1 (GBA1) represent the most prevalent risk factor for Parkinson's disease. The molecular mechanisms underlying the link between GBA1 mutations and Parkinson's disease are incompletely understood. We analysed two aged (24-month-old) Gba1 mouse models, one carrying a knock-out mutation and the other a L444P knock-in mutation. A significant reduction of glucocerebrosidase activity was associated with increased total alpha-synuclein accumulation in both these models. Gba1 mutations alone did not alter the number of nigral dopaminergic neurons nor striatal dopamine levels. We then investigated the effect of overexpression of human alpha-synuclein in the substantia nigra of aged (18 to 21-month-old) L444P Gba1 mice. Following intraparenchymal injections of human alpha-synuclein carrying viral vectors, pathological accumulation of phosphorylated alpha-synuclein occurred within the transduced neurons. Stereological counts of nigral dopaminergic neurons revealed a significantly greater cell loss in Gba1-mutant than wild-type mice. These results indicate that Gba1 deficiency enhances neuronal vulnerability to neurodegenerative processes triggered by increased alpha-synuclein expression.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Glucosilceramidase/genética
Mutação/genética
Neurônios/patologia
Substância Negra/patologia
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Encéfalo/metabolismo
Encéfalo/patologia
Glucosilceramidase/deficiência
Seres Humanos
Leucina/genética
Camundongos
Camundongos Transgênicos
Neurônios/metabolismo
Prolina/genética
Desempenho Psicomotor/fisiologia
Olfato/genética
Substância Negra/metabolismo
Transdução Genética
Tirosina 3-Mono-Oxigenase/metabolismo
beta-N-Acetil-Hexosaminidases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (alpha-Synuclein); 9DLQ4CIU6V (Proline); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 3.2.1.45 (Glucosylceramidase); EC 3.2.1.52 (beta-N-Acetylhexosaminidases); GMW67QNF9C (Leucine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx221


  10 / 13990 MEDLINE  
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[PMID]:28939041
[Au] Autor:Kim H; Kang H; Lee Y; Park CH; Jo A; Khang R; Shin JH
[Ad] Endereço:Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, South Korea; HuGeX Co., Ltd., Seongnam 462-122, South Korea.
[Ti] Título:Identification of transketolase as a target of PARIS in substantia nigra.
[So] Source:Biochem Biophys Res Commun;493(2):1050-1056, 2017 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recently, PARIS (ZNF746) is introduced as authentic substrate of parkin and transcriptionally represses PGC-1α by binding to insulin responsive sequences (IRSs) in the promoter of PGC-1α. The overexpression of PARIS selectively leads to the loss of dopaminergic neurons (DN) and mitochondrial abnormalities in the substantia nigra (SN) of Parkinson's disease (PD) models. To identify PARIS target molecules altered in SN region-specific manner, LC-MS/MS-based quantitative proteomic analysis is employed to investigate proteomic alteration in the cortex, striatum, and SN of AAV-PARIS injected mice. Herein, we find that the protein and mRNA of transketolase (TKT), a key enzyme in pentose phosphate pathway (PPP) of glucose metabolism, is exclusively decreased in the SN of AAV-PARIS mice. PARIS overexpression suppresses TKT transcription via IRS-like motif in the TKT promoter. Moreover, the reduction of TKT by PARIS is found in primary DN but not in cortical neurons, suggesting that PARIS-medicated TKT suppression is cell type-dependent. Interestingly, we observe the reduced level of TKT in the SN of PD patients but not in the cortex. These findings indicate that TKT might be a SN-specific target of PARIS, providing new clues to understand the mechanism underlying selective DNs death in PD.
[Mh] Termos MeSH primário: Proteínas Repressoras/metabolismo
Substância Negra/metabolismo
Transcetolase/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Linhagem Celular Tumoral
Células Cultivadas
Regulação da Expressão Gênica
Glicólise
Seres Humanos
Camundongos
Doença de Parkinson/genética
Doença de Parkinson/metabolismo
Doença de Parkinson/patologia
Via de Pentose Fosfato
Proteômica
Ratos
Proteínas Repressoras/análise
Proteínas Repressoras/genética
Substância Negra/patologia
Transcetolase/análise
Transcetolase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Repressor Proteins); 0 (ZNF746 protein, mouse); EC 2.2.1.1 (Transketolase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE



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