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[PMID]: 28467342 [Au] Autor: Zarola F [Ad] Endereço: Parkinson's Disease Clinical Center Azienda Sanitaria Locale RM H Via Gallerie di Sotto, snc Albano Laziale Roma. florazarola@libero.it. [Ti] Título: Incidence of vascular brain damage in a population with Parkinson Disease: a clinical statistic study in comparison with a control group of patients afferent to neurological movement disorder outpatients clinic. [So] Source: Acta Biomed;88(1):95-96, 2017 Apr 28. [Is] ISSN: 0392-4203 [Cp] País de publicação: Italy [La] Idioma: eng [Ab] Resumo: N/A. [Mh] Termos MeSH primário: Infarto Encefálico/diagnóstico Doença de Parkinson Secundária/complicações [Mh] Termos MeSH secundário: Idoso Idoso de 80 Anos ou mais Estudos de Casos e Controles Feminino Seres Humanos Masculino Meia-Idade [Pt] Tipo de publicação: JOURNAL ARTICLE [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180125 [Lr] Data última revisão: 180125 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170504 [St] Status: MEDLINE [do] DOI: 10.23750/abm.v88i1.5008

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[PMID]: 28455267 [Au] Autor: Xi SS; Bai XX; Gu L; Bao LH; Yang HM; An W; Wang XM; Zhang H [Ad] Endereço: Department of Neurobiology, School of Basic Medical Sciences, Beijing Institute for Brain Disorders and Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University, Beijing 100069, China. [Ti] Título: Metabotropic glutamate receptor 5 mediates the suppressive effect of 6-OHDA-induced model of Parkinson's disease on liver cancer. [So] Source: Pharmacol Res;121:145-157, 2017 Jul. [Is] ISSN: 1096-1186 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: Numerous epidemiological studies suggested that there is a variable cancer risk in patients with Parkinson's disease (PD). However, the underlying mechanisms remain unclear. In the present study, the role of metabotropic glutamate receptor 5 (mGluR5) has been investigated in 6-hydroxydopamine (6-OHDA)-induced PD combined with liver cancer both in vitro and in vivo. We found that PD cellular model from 6-OHDA-lesioned MN9D cells suppressed the growth, migration, and invasion of Hepa1-6 cells via down-regulation of mGluR5-mediated ERK and Akt pathway. The application of 2-methyl-6-(phenylethyl)-pyridine and knockdown of mGluR5 further decreased the effect on Hepa-1-6 cells when co-cultured with conditioned media. The effect was increased by (S)-3,5-dihydroxyphenylglycine and overexpression of mGluR5. Moreover, more release of glutamate from 6-OHDA-lesioned MN9D cells suppressed mGluR5-mediated effect of Hepa1-6 cells. Application of riluzole eliminated the increased glutamate release induced by 6-OHDA in MN9D cells and aggravated the suppressive effect on Hepa-1-6 cells. In addition, the growth of implanted liver cancer was inhibited in 6-OHDA induced PD-like rats, and was associated with increased glutamate release in the serum and down-regulation of mGluR5 in tumor tissue. Collectively, these results indicate that selective antagonism of glutamate and mGluR5 has a potentially beneficial effect in both liver cancer and PD, and thus may provide more understanding for the clinical investigation and further an additional therapeutic target for these two diseases. [Mh] Termos MeSH primário: Ácido Glutâmico/metabolismo Neoplasias Hepáticas/metabolismo Oxidopamina Doença de Parkinson Secundária/metabolismo Receptor de Glutamato Metabotrópico 5/metabolismo [Mh] Termos MeSH secundário: Animais Linhagem Celular Tumoral Movimento Celular Proliferação Celular Modelos Animais de Doenças Fígado/metabolismo Fígado/patologia Neoplasias Hepáticas/patologia Sistema de Sinalização das MAP Quinases Masculino Camundongos Doença de Parkinson Secundária/patologia Proteínas Proto-Oncogênicas c-akt/metabolismo Ratos Sprague-Dawley [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Receptor, Metabotropic Glutamate 5); 3KX376GY7L (Glutamic Acid); 8HW4YBZ748 (Oxidopamine); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180105 [Lr] Data última revisão: 180105 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170430 [St] Status: MEDLINE

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[PMID]: 29191452 [Au] Autor: Poetini MR; Araujo SM; Trindade de Paula M; Bortolotto VC; Meichtry LB; Polet de Almeida F; Jesse CR; Kunz SN; Prigol M [Ad] Endereço: Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas- LaftamBio Pampa- Universidade Federal do Pampa, Itaqui, CEP 97650-000, RS, Brazil. [Ti] Título: Hesperidin attenuates iron-induced oxidative damage and dopamine depletion in Drosophila melanogaster model of Parkinson's disease. [So] Source: Chem Biol Interact;279:177-186, 2018 Jan 05. [Is] ISSN: 1872-7786 [Cp] País de publicação: Ireland [La] Idioma: eng [Ab] Resumo: This study has evaluated the action of flavonoid hesperidin on the neurotoxic effects caused by the intake of iron (Fe) in Drosophila melanogaster. Male adult flies, aged 1-3 days, have been divided into four groups of 50 each: (1) control, (2) Hsd 10 µM, (3) Fe 20 mM (4) Hsd 10 µM + Fe 20 mM. During the exposure protocol, the flies have been exposed to a diet containing Hsd and/or Fe for 48 h. The survival and behavioral analyses have been carried out in vivo, and ex vivo. The analyses involved acetylcholinesterase (AChE) activity and Fe levels in the flies' heads and bodies and determination of dopaminergic levels, cellular and mitochondrial viability, activities of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), reactive species levels (RS), thiobarbituric acid reactive substances (TBARS) and contents of total thiols and non-proteic thiols (NPSH) in the flies' heads. A significant negative correlation between Fe levels in the head of the flies and the survival, dopamine levels and antioxidant enzymes in the head of the flies has been found. Additionally, significant positive correlation between Fe levels in the head of the flies with negative geotaxis RS and AChE activity in the head of the flies has been found. It demonstrates that the flies which had higher levels of Fe in their heads have demonstrated more susceptibility to neurotoxicity. An important result from our study is that Hsd treatment promotes a decrease in Fe concentration in the head, restores dopamine levels and cholinergic activity of the flies and improves motor function caused by Fe. Hsd also ameliorates Fe induced mortality, oxidative stress and mitochondrial dysfunction. Our results have demonstrated the neuroprotective effect of Hsd and it suggests that flavonoid acts in different ways to protect against the Parkinson disease caused by Fe exposure such as the direct scavenging of RS and activation of antioxidant enzymes. [Mh] Termos MeSH primário: Dopamina/metabolismo Drosophila melanogaster/efeitos dos fármacos Hesperidina/farmacologia Ferro/toxicidade Estresse Oxidativo/efeitos dos fármacos Doença de Parkinson Secundária/induzido quimicamente [Mh] Termos MeSH secundário: Animais Biomarcadores Masculino Metalotioneína/metabolismo Mitocôndrias Atividade Motora/efeitos dos fármacos Oxirredução Doença de Parkinson Secundária/prevenção & controle [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Biomarkers); 9038-94-2 (Metallothionein); E1UOL152H7 (Iron); E750O06Y6O (Hesperidin); VTD58H1Z2X (Dopamine) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180103 [Lr] Data última revisão: 180103 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 171202 [St] Status: MEDLINE

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[PMID]: 27776889 [Au] Autor: Dahl R [Ad] Endereço: Neurodon LLC, 5700 Tanager St., Schererville, IN 46375, USA. Electronic address: rdahl@neurodon.net. [Ti] Título: A new target for Parkinson's disease: Small molecule SERCA activator CDN1163 ameliorates dyskinesia in 6-OHDA-lesioned rats. [So] Source: Bioorg Med Chem;25(1):53-57, 2017 01 01. [Is] ISSN: 1464-3391 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Endoplasmic reticulum (ER) stress is intimately linked to Parkinson's disease (PD) pathophysiology. Disrupted intracellular calcium homeostasis is a major cause of the ER stress seen in dopaminergic neurons, leading to the cell death and subsequent loss of movement and coordination in patients. Dysfunctional calcium handling proteins play a major role in the promulgation of ER stress in PD. Specifically, compromised sarco/endoplasmic reticulum Ca -ATPase (SERCA) has been identified as a major cause of ER stress and neuron loss in PD. We have identified a small molecule activator of SERCA that increases ER calcium content, rescues neurons from ER stress-induced cell death in vitro, and shows significant efficacy in the rat 6-hydroxydopamine (6-OHDA) model of PD. Together, these results support targeting SERCA activation as a viable strategy to develop disease-modifying therapeutics for PD. [Mh] Termos MeSH primário: Aminoquinolinas/uso terapêutico Benzamidas/uso terapêutico Discinesias/tratamento farmacológico Ativadores de Enzimas/uso terapêutico Oxidopamina Doença de Parkinson Secundária/tratamento farmacológico ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo [Mh] Termos MeSH secundário: Animais Cálcio/metabolismo Morte Celular/efeitos dos fármacos Descoberta de Drogas Discinesias/complicações Discinesias/metabolismo Estresse do Retículo Endoplasmático/efeitos dos fármacos Masculino Doença de Parkinson Secundária/complicações Doença de Parkinson Secundária/metabolismo Ratos Ratos Wistar [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Aminoquinolines); 0 (Benzamides); 0 (CDN1163); 0 (Enzyme Activators); 8HW4YBZ748 (Oxidopamine); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); SY7Q814VUP (Calcium) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 171207 [Lr] Data última revisão: 171207 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161026 [St] Status: MEDLINE

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[PMID]: 28800639 [Au] Autor: López A; Ortiz F; Doerrier C; Venegas C; Fernández-Ortiz M; Aranda P; Díaz-Casado ME; Fernández-Gil B; Barriocanal-Casado E; Escames G; López LC; Acuña-Castroviejo D [Ad] Endereço: Instituto de Biotecnología, Centro de Investigación Biomédica, Parque Tecnológico de Ciencias de la Salud, and Departamento de Fisiología, Facultad de Medicina, Universidad de Granada, Granada, Spain. [Ti] Título: Mitochondrial impairment and melatonin protection in parkinsonian mice do not depend of inducible or neuronal nitric oxide synthases. [So] Source: PLoS One;12(8):e0183090, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: MPTP-mouse model constitutes a well-known model of neuroinflammation and mitochondrial failure occurring in Parkinson's disease (PD). Although it has been extensively reported that nitric oxide (NOâ—�) plays a key role in the pathogenesis of PD, the relative roles of nitric oxide synthase isoforms iNOS and nNOS in the nigrostriatal pathway remains, however, unclear. Here, the participation of iNOS/nNOS isoforms in the mitochondrial dysfunction was analyzed in iNOS and nNOS deficient mice. Our results showed that MPTP increased iNOS activity in substantia nigra and striatum, whereas it sharply reduced complex I activity and mitochondrial bioenergetics in all strains. In the presence of MPTP, mice lacking iNOS showed similar restricted mitochondrial function than wild type or mice lacking nNOS. These results suggest that iNOS-dependent elevated nitric oxide, a major pathological hallmark of neuroinflammation in PD, does not contribute to mitochondrial impairment. Therefore, neuroinflammation and mitochondrial dysregulation seem to act in parallel in the MPTP model of PD. Melatonin administration, with well-reported neuroprotective properties, counteracted these effects, preventing from the drastic changes in mitochondrial oxygen consumption, increased NOS activity and prevented reduced locomotor activity induced by MPTP. The protective effects of melatonin on mitochondria are also independent of its anti-inflammatory properties, but both effects are required for an effective anti-parkinsonian activity of the indoleamine as reported in this study. [Mh] Termos MeSH primário: Melatonina/farmacologia Mitocôndrias/efeitos dos fármacos Fármacos Neuroprotetores/farmacologia Óxido Nítrico Sintase Tipo II/genética Óxido Nítrico Sintase Tipo I/genética Doença de Parkinson Secundária/tratamento farmacológico [Mh] Termos MeSH secundário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina Animais Corpo Estriado/efeitos dos fármacos Corpo Estriado/metabolismo Corpo Estriado/patologia Regulação da Expressão Gênica Masculino Camundongos Camundongos Endogâmicos C57BL Camundongos Knockout Mitocôndrias/metabolismo Mitocôndrias/patologia Neurônios/efeitos dos fármacos Neurônios/metabolismo Neurônios/patologia Óxido Nítrico/metabolismo Óxido Nítrico Sintase Tipo I/deficiência Óxido Nítrico Sintase Tipo II/deficiência Consumo de Oxigênio/efeitos dos fármacos Doença de Parkinson Secundária/induzido quimicamente Doença de Parkinson Secundária/genética Doença de Parkinson Secundária/patologia Substância Negra/efeitos dos fármacos Substância Negra/metabolismo Substância Negra/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Neuroprotective Agents); 31C4KY9ESH (Nitric Oxide); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos1 protein, mouse); EC 1.14.13.39 (Nos2 protein, mouse); JL5DK93RCL (Melatonin) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171006 [Lr] Data última revisão: 171006 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170812 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0183090

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[PMID]: 28781257 [Au] Autor: Kryukova EV; Shelukhina IV; Kolacheva AA; Alieva AK; Shadrina MI; Slominsky PA; Kasheverov IE; Utkin YN; Ugrumov MV; Tsetlin VI [Ad] Endereço: Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences. [Ti] Título: [Possible involvement of neuronal nicotinic acetylcholine receptors in compensatory brain mechanisms at early stages of Parkinson's disease]. [Ti] Título: Vozmozhnoe uchastie neironal'nykh nikotinovykh atsetilkholinovykh retseptorov v kompensatornykh mekhanizmakh mozga na rannikh stadiiakh bolezni Parkinsona.. [So] Source: Biomed Khim;63(3):241-247, 2017 May. [Is] ISSN: 2310-6972 [Cp] País de publicação: Russia (Federation) [La] Idioma: rus [Ab] Resumo: A role of nicotinic acetylcholine receptors (nAChR) in the development of Parkinson's disease (PD) has been investigated using two mouse models corresponding to the presymptomatic stage and the early symptomatic stage of PD. Quantitative determination of nAChR in the striatum and substantia nigra (SN) was performed using the radioactive derivatives of epibatidine, ï�¡-conotoxin MII, and ï�¡-bungarotoxin as ligands. The number of ligand-binding sites changed differently depending on their location in the brain, the stage of the disease and the receptor subtype. Epibatidine binding decreased in the striatum to 66% and 70% at the presymptomatic and early symptomatic stages, respectively, whereas in SN a 160% increase was registered at the presymptomatic stage. The ï�¡-conotoxin MII binding on striatal dopaminergic axonal terminals at the presymptomatic stage decreased by 20% and at the symptomatic stage it demonstrated a further decrease. The increase in ï�¡-bungarotoxin binding at the presymptomatic stage and a decrease at the early symptomatic stage was observed in the striatum. In SN, the level of ï�¡-bungarotoxin binding decreased at the presymptomatic stage and kept constant at the symptomatic stage. The significant decrease in the expression of Chrna4 and Chrna6 genes encoding ï�¡4 and ï�¡6 nAChR subunits was observed in SN at the early symptomatic stage, while a 13-fold increase in expression of the Chrna7 gene encoding the ï�¡7 nAChR subunit was detected at the presymptomatic stage. The data obtained suggest possible involvement of nAChR in compensatory mechanisms at early PD stages. [Mh] Termos MeSH primário: Corpo Estriado/metabolismo Doença de Parkinson Secundária/genética Receptores Nicotínicos/genética Substância Negra/metabolismo Receptor Nicotínico de Acetilcolina alfa7/genética [Mh] Termos MeSH secundário: Animais Doenças Assintomáticas Sítios de Ligação Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia Bungarotoxinas/farmacologia Conotoxinas/farmacologia Corpo Estriado/efeitos dos fármacos Corpo Estriado/fisiopatologia Modelos Animais de Doenças Progressão da Doença Regulação da Expressão Gênica Seres Humanos Ligantes Camundongos Agonistas Nicotínicos/farmacologia Especificidade de Órgãos Doença de Parkinson Secundária/metabolismo Doença de Parkinson Secundária/fisiopatologia Ligação Proteica Isoformas de Proteínas/genética Isoformas de Proteínas/metabolismo Piridinas/farmacologia RNA Mensageiro/genética RNA Mensageiro/metabolismo Receptores Nicotínicos/metabolismo Transdução de Sinais Substância Negra/efeitos dos fármacos Substância Negra/fisiopatologia Receptor Nicotínico de Acetilcolina alfa7/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Bungarotoxins); 0 (Chrna7 protein, mouse); 0 (Conotoxins); 0 (Ligands); 0 (Nicotinic Agonists); 0 (Protein Isoforms); 0 (Pyridines); 0 (RNA, Messenger); 0 (Receptors, Nicotinic); 0 (alpha7 Nicotinic Acetylcholine Receptor); 0 (nicotinic acetylcholine receptor alpha4 subunit); M6K314F1XX (epibatidine) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170912 [Lr] Data última revisão: 170912 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170808 [St] Status: MEDLINE [do] DOI: 10.18097/PBMC20176303241

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[PMID]: 28777965 [Au] Autor: Cicero CE; Mostile G; Vasta R; Rapisarda V; Signorelli SS; Ferrante M; Zappia M; Nicoletti A [Ad] Endereço: Department of Medical, Surgical Sciences and Advanced Technologies "G. F. Ingrassia", University of Catania, Catania, Italy. [Ti] Título: Metals and neurodegenerative diseases. A systematic review. [So] Source: Environ Res;159:82-94, 2017 11. [Is] ISSN: 1096-0953 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: Neurodegenerative processes encompass a large variety of diseases with different pathological patterns and clinical presentation such as Amyotrophic Lateral Sclerosis (ALS), Alzheimer Disease (AD) and Parkinson's disease (PD). Genetic mutations have a known causative role, but the majority of cases are likely to be probably caused by a complex gene-environment interaction. Exposure to metals has been hypothesized to increase oxidative stress in brain cells leading to cell death and neurodegeneration. Neurotoxicity of metals has been demonstrated by several in vitro and in vivo experimental studies and it is likely that each metal could be toxic through specific pathways. The possible pathogenic role of different metals has been supported by some epidemiological evidences coming from occupational and ecological studies. In order to assess the possible association between metals and neurodegenerative disorders, several case-control studies have also been carried out evaluating the metals concentration in different biological specimens such as blood/serum/plasma, cerebrospinal fluid (CSF), nail and hair, often reporting conflicting results. This review provides an overview of our current knowledge on the possible association between metals and ALS, AD and PD as main neurodegenerative disorders. [Mh] Termos MeSH primário: Doença de Alzheimer/epidemiologia Esclerose Amiotrófica Lateral/epidemiologia Poluentes Ambientais/toxicidade Metais/toxicidade Doença de Parkinson Secundária/epidemiologia [Mh] Termos MeSH secundário: Doença de Alzheimer/induzido quimicamente Esclerose Amiotrófica Lateral/induzido quimicamente Seres Humanos Doença de Parkinson Secundária/induzido quimicamente [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Environmental Pollutants); 0 (Metals) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171120 [Lr] Data última revisão: 171120 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170805 [St] Status: MEDLINE

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[PMID]: 28688763 [Au] Autor: Go S; Kurita H; Yokoo K; Inden M; Kambe T; Hozumi I [Ad] Endereço: Laboratory of Medical Therapeutics and Molecular Therapeutics, Department Biomedical Pharmaceutics, Gifu Pharmaceutical University, 1-25-4 Daigaku-nishi Gifu City, Gifu 501-1196, Japan. [Ti] Título: Protective function of SLC30A10 induced via PERK-ATF4 pathway against 1-methyl-4-phenylpyridinium. [So] Source: Biochem Biophys Res Commun;490(4):1307-1313, 2017 Sep 02. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Solute carrier family 30 member 10 (SLC30A10) has been known as manganese transporter. It has been suggested that neurodegenerative diseases are related with cellular stress such as oxidative stress or endoplasmic reticulum (ER) stress. However, it remains unknown whether SLC30A10 is actually involved in several intracellular stress. We found that the level of Slc30a10 was increased in midbrain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Therefore, we further investigated the role of SLC30A10 in the 1-methyl-4-phenylpiridium ion (MPP )-induced intracellular stress, and the molecular mechanism underlying SLC30A10 induction by MPP treatment. In human neuroblastoma cell line (SH-SY5Y) treated with MPP (1 mM), the SLC30A10 mRNA level was significantly increased, and in addition, the expression of CHOP, which is known as one of ER stress markers, was significantly increased by MPP . Interestingly, the level of SLC30A10 mRNA was significantly increased by tunicamycin as an ER stressor, suggesting that the induction of SLC30A10 by MPP was caused via ER stress. Considering that PKR-like endoplasmic reticulum kinase (PERK) pathway is activated under ER stress induced by MPP , we investigated whether the expression of SLC30A10 is increased through ATF4, which is major transcription factor in PERK pathway. The increase of SLC30A10 expression in MPP -treated cells was eliminated by ATF4 knockdown. And the protective role of SLC30A10 against MPP -induced ER stress was confirmed by measuring cell viability in SLC30A10 knockdown cells. In conclusion, SLC30A10 is thought to have protective role for MPP -induced toxicity via PERK-ATF4 pathway. [Mh] Termos MeSH primário: 1-Metil-4-fenilpiridínio/farmacologia Fator 4 Ativador da Transcrição/genética Proteínas de Transporte de Cátions/genética Retículo Endoplasmático/metabolismo Doença de Parkinson Secundária/genética eIF-2 Quinase/genética [Mh] Termos MeSH secundário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina/farmacologia Fator 4 Ativador da Transcrição/antagonistas & inibidores Fator 4 Ativador da Transcrição/metabolismo Animais Proteínas de Transporte de Cátions/metabolismo Linhagem Celular Tumoral Sobrevivência Celular/efeitos dos fármacos Retículo Endoplasmático/efeitos dos fármacos Estresse do Retículo Endoplasmático/efeitos dos fármacos Regulação da Expressão Gênica Seres Humanos Masculino Mesencéfalo/efeitos dos fármacos Mesencéfalo/metabolismo Mesencéfalo/patologia Camundongos Camundongos Endogâmicos C57BL Neurônios/efeitos dos fármacos Neurônios/metabolismo Neurônios/patologia Doença de Parkinson Secundária/induzido quimicamente Doença de Parkinson Secundária/metabolismo Doença de Parkinson Secundária/patologia Isoformas de Proteínas/genética Isoformas de Proteínas/metabolismo RNA Interferente Pequeno/genética RNA Interferente Pequeno/metabolismo Fator de Transcrição CHOP/genética Fator de Transcrição CHOP/metabolismo Tunicamicina/farmacologia Transportador 8 de Zinco eIF-2 Quinase/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (ATF4 protein, human); 0 (Cation Transport Proteins); 0 (DDIT3 protein, human); 0 (Protein Isoforms); 0 (RNA, Small Interfering); 0 (SLC30A8 protein, human); 0 (Zinc Transporter 8); 11089-65-9 (Tunicamycin); 145891-90-3 (Activating Transcription Factor 4); 147336-12-7 (Transcription Factor CHOP); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); EC 2.7.11.1 (EIF2AK3 protein, human); EC 2.7.11.1 (eIF-2 Kinase); R865A5OY8J (1-Methyl-4-phenylpyridinium) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170710 [St] Status: MEDLINE

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[PMID]: 28622392 [Au] Autor: Wang L; Wang Z; Zhu R; Bi J; Feng X; Liu W; Wu J; Zhang H; Wu H; Kong W; Yu B; Yu X [Ad] Endereço: National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun, Jilin Province, China. [Ti] Título: Therapeutic efficacy of AAV8-mediated intrastriatal delivery of human cerebral dopamine neurotrophic factor in 6-OHDA-induced parkinsonian rat models with different disease progression. [So] Source: PLoS One;12(6):e0179476, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Parkinson's disease (PD) is a progressive and age-associated neurodegenerative disorder. Patients at different stages of the disease course have distinguished features, mainly in the number of dopaminergic neurons. Cerebral dopamine neurotrophic factor (CDNF) is a recently discovered neurotrophic factor, being deemed as a hopeful candidate for PD treatment. Here, we evaluated the efficacy of CDNF in protecting dopaminergic function using the 6-OHDA-induced PD rat model suffering from different levels of neuronal loss and the recombinant adeno-associated virus 8 (AAV8) as a carrier for the CDNF gene. The results showed that AAV8-CDNF administration significantly improved the motor function and increased the tyrosine hydroxylase (TH) levels in PD rats with mild lesions (2 weeks post lesion), but it had limited therapeutic effects in rats with severe lesions (5 weeks post lesion). To better improve the recovery of motor function in severely lesioned PD rats, we employed a strategy using the CDNF gene along with the aromatic amino acid decarboxylase (AADC) gene. This combination therapeutic strategy indeed showed an enhanced benefit in restoring the motor function of severely lesioned PD rats by providing the neuroprotective effect of CDNF and dopamine enhancing effect of AADC as expected. This study may provide a basis for future clinical application of CDNF in PD patients at different stages and offer a new alternative strategy of joint use of CDNF and AADC for advanced PD patients in clinical trials. [Mh] Termos MeSH primário: Corpo Estriado Dependovirus Terapia Genética/métodos Atividade Motora Fatores de Crescimento Neural Oxidopamina/efeitos adversos Doença de Parkinson Secundária Recuperação de Função Fisiológica Transdução Genética/métodos [Mh] Termos MeSH secundário: Animais Descarboxilases de Aminoácido-L-Aromático/biossíntese Descarboxilases de Aminoácido-L-Aromático/genética Corpo Estriado/metabolismo Corpo Estriado/fisiopatologia Seres Humanos Masculino Fatores de Crescimento Neural/biossíntese Fatores de Crescimento Neural/genética Oxidopamina/farmacologia Doença de Parkinson Secundária/induzido quimicamente Doença de Parkinson Secundária/genética Doença de Parkinson Secundária/metabolismo Doença de Parkinson Secundária/terapia Ratos Ratos Wistar [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (CDNF protein, human); 0 (Nerve Growth Factors); 8HW4YBZ748 (Oxidopamine); EC 4.1.1.28 (Aromatic-L-Amino-Acid Decarboxylases); EC 4.1.1.28 (DDC protein, human) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170914 [Lr] Data última revisão: 170914 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170617 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0179476

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[PMID]: 28598268 [Au] Autor: Krajnak K; Sriram K; Johnson C; Roberts JR; Mercer R; Miller GR; Wirth O; Antonini JM [Ad] Endereço: a Engineering Controls and Technology Branch, National Institute for Occupational Safety and Health , Morgantown , WV , USA. [Ti] Título: Effects of pulmonary exposure to chemically-distinct welding fumes on neuroendocrine markers of toxicity. [So] Source: J Toxicol Environ Health A;80(5):301-314, 2017. [Is] ISSN: 1528-7394 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Exposure to welding fumes may result in disorders of the pulmonary, cardiovascular, and reproductive systems. Welders are also at a greater risk of developing symptoms similar to those seen in individuals with idiopathic Parkinson's disease. In welders, there are studies that suggest that alterations in circulating prolactin concentrations may be indicative of injury to the dopamine (DA) neurons in the substantia nigra. The goal of these studies was to use an established model of welding particulate exposure to mimic the effects of welding fume inhalation on reproductive functions. Since previous investigators suggested that changes in circulating prolactin may be an early marker of DA neuron injury, movement disorders, and reproductive dysfunction, prolactin, hypothalamic tyrosine hydroxylase (TH) levels (a marker of DA synthesis), and other measures of hypothalamic-pituitary-gonadal (HPG) function were measured after repetitive instillation of welding fume particulates generated by flux core arc-hard surfacing (FCA-HS), manual metal arc-hard surfacing (MMA-HS) or gas metal arc-mild steel (GMA-MS) welding, or manganese chloride (MnCl ). Exposure to welding fume particulate resulted in the accumulation of various metals in the pituitary and testes of rats, along with changes in hypothalamic TH and serum prolactin levels. Exposure to particulates with high concentrations of soluble manganese (Mn) appeared to exert the greatest influence on TH activity levels and serum prolactin concentrations. Thus, circulating prolactin levels may serve as a biomarker for welding fume/Mn-induced neurotoxicity. Other reproductive measures were collected, and these data were consistent with epidemiological findings that prolactin and testosterone may serve as biomarkers of welding particulate induced DA neuron and reproductive dysfunction. [Mh] Termos MeSH primário: Poluentes Ocupacionais do Ar/toxicidade Biomarcadores/sangue Exposição por Inalação Manganês/toxicidade Exposição Ocupacional Soldagem [Mh] Termos MeSH secundário: Animais Biomarcadores/metabolismo Cloretos/toxicidade Hipotálamo/enzimologia Masculino Compostos de Manganês Doença de Parkinson Secundária/induzido quimicamente Prolactina/sangue Ratos Ratos Sprague-Dawley Reprodução/efeitos dos fármacos Espermatogênese/efeitos dos fármacos Testosterona/metabolismo Tirosina 3-Mono-Oxigenase/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Air Pollutants, Occupational); 0 (Biomarkers); 0 (Chlorides); 0 (Manganese Compounds); 3XMK78S47O (Testosterone); 42Z2K6ZL8P (Manganese); 9002-62-4 (Prolactin); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); QQE170PANO (manganese chloride) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 170707 [Lr] Data última revisão: 170707 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170610 [St] Status: MEDLINE [do] DOI: 10.1080/15287394.2017.1318324

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