Journal of Neurodegenerative Diseases最新文献

{"title":"Visual Evoked Potentials in Primary Open Angle Glaucoma.","authors":"Mukesh Kumar Jha,&nbsp;Dilip Thakur,&nbsp;Nirmala Limbu,&nbsp;Badri Prasad Badhu,&nbsp;Bishnu Hari Paudel","doi":"10.1155/2017/9540609","DOIUrl":"https://doi.org/10.1155/2017/9540609","url":null,"abstract":"<p><strong>Background and aims: </strong>Visual evoked potentials (VEPs) assess the integrity of the visual pathways from the optic nerve to the occipital cortex. Optic disc cupping and visual field loss have been associated with prolongation of latency of VEP in primary open angle glaucoma (POAG).</p><p><strong>Methods: </strong>Pattern reversal and flash VEP tests were done in consenting 20 primary open angle glaucoma eyes and 40 normal control eyes.</p><p><strong>Results: </strong>In POAG cases, the refractive error [3.51 ± 1.88 versus 1.88 ± 1.11, D, <i>p</i> = 0.001], cup-disc ratio in percent [66.00 ± 16.98 versus 28.50 ± 5.80, <i>p</i> = 0.001], intraocular pressure [19.55 ± 2.08 versus 11.65 ± 1.64, mmHg, <i>p</i> = 0.001], and automated visual field pattern standard deviation [4.13 ± 6.96 versus 1.64 ± 0.45, dB, <i>p</i> = 0.001] were significantly more than in control. The visual acuity [0.41 ± 0.29 versus 1.00 ± 0.00, <i>p</i> = 0.001], foveal visual sensitivity [25.92 ± 6.88 versus 33.48 ± 1.75, dB, <i>p</i> = 0.001], and automated visual field mean deviation [-9.63 ± 10.58 versus 0.07 ± 1.54, dB, <i>p</i> = 0.001] were significantly less in cases than in control. Among VEP variables, pattern reversal latency N145 [149.00 ± 15.75 versus 137.52 ± 15.20, ms, <i>p</i> = 0.011], flash amplitude N75 [2.18 ± .57 versus 1.47 ± .38, <i>μ</i>V, <i>p</i> = 0.001], and flash amplitude N145 [1.99 ± .39 versus 1.43 ± .38, <i>μ</i>V, <i>p</i> = 0.001] were increased in cases. The pattern reversal amplitude N75 [1.97 ± .35 versus 2.47 ± .58, <i>μ</i>V, <i>p</i> = 0.001], amplitude P100 [3.09 ± .46 versus 6.07 ± 1.44, <i>μ</i>V, <i>p</i> = 0.001], and amplitude N145 [2.21 ± .58 versus 4.45 ± 1.99, <i>μ</i>V, <i>p</i> = 0.001] were decreased in cases.</p><p><strong>Conclusions: </strong>POAG caused glaucomatous damage to optic pathway.</p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2017 ","pages":"9540609"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2017/9540609","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35319435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of Resistance Training on Neuromuscular Function and Physical Capacity in ALS Patients.","authors":"L Jensen,&nbsp;J B Djurtoft,&nbsp;R D Bech,&nbsp;J L Nielsen,&nbsp;L H Jørgensen,&nbsp;H D Schrøder,&nbsp;U Frandsen,&nbsp;P Aagaard,&nbsp;L G Hvid","doi":"10.1155/2017/1436519","DOIUrl":"https://doi.org/10.1155/2017/1436519","url":null,"abstract":"<p><strong>Objectives: </strong>The present study aimed to explore the effect of resistance training in patients with amyotrophic lateral sclerosis (ALS), a disease characterized by progressive motor neuron loss and muscle weakness.</p><p><strong>Materials and methods: </strong>Following a 12-week \"lead-in\" control period, a population of ALS patients from Funen, Denmark, completed a 12-week resistance training program consisting of 2-3 sessions/week. Neuromuscular function (strength and power) and voluntary muscle activation (superimposed twitch technique) were evaluated before and after both control and training periods. Physical capacity tests (chair rise and timed up and go), the revised ALS functional rating scale (ALSFRS-R) scores, and muscle cross sectional area (histology) were also assessed.</p><p><strong>Results: </strong>Of twelve ALS patients assessed for eligibility, six were included and five completed the study. Training did not significantly affect the ALSFRS-R score, and loss of neuromuscular function (strength and power) increased following the training period. However, an improved functionality (chair rise) and an increase in greatly hypertrophied type II fibres combined with an increase in atrophied fibres following the training period compared to the control period were observed.</p><p><strong>Conclusion: </strong>In this small study, the present form of resistance training was unable to attenuate progressive loss of neuromuscular function in ALS, despite some changes in physical capacity and morphology.</p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2017 ","pages":"1436519"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2017/1436519","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35073630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Analysis of Algerian Patients with Pompe Disease.","authors":"Y Sifi,&nbsp;M Medjroubi,&nbsp;R Froissart,&nbsp;N Taghane,&nbsp;K Sifi,&nbsp;A Benhabiles,&nbsp;S Lemai,&nbsp;S Semra,&nbsp;H Benmekhebi,&nbsp;Z Bouderda,&nbsp;N Abadi,&nbsp;A Hamri","doi":"10.1155/2017/9427269","DOIUrl":"https://doi.org/10.1155/2017/9427269","url":null,"abstract":"<p><p>Pompe's disease is a metabolic myopathy caused by a deficiency of acid alpha-glucosidase (GAA), also called acid maltase, an enzyme that degrades lysosomal glycogen. The clinical presentation of Pompe's disease is variable with respect to the age of onset and rate of disease progression. Patients with onset of symptoms in early infancy (infantile-onset Pompe disease (IOPD)) typically exhibit rapidly progressive hypertrophic cardiomyopathy and marked muscle weakness. Most of them die within the first year of life from cardiac and/or respiratory failure. In the majority of cases of Pompe's disease, onset of symptoms occurs after infancy, ranging widely from the first to sixth decade of life (late-onset Pompe's disease or LOPD). Progression of the disease is relentless and patients eventually progress to loss of ambulation and death due to respiratory failure. The objective of this study was to characterize the clinical presentation of 6 patients (3 with EOPD and the other 3 with LOPD) of 5 families from the East of Algeria. All our patients were diagnosed as having Pompe's disease based on biochemical confirmations of GAA deficiency by dried blood spots (DBS) and GAA gene mutations were analyzed in all patients who consented (<i>n</i> = 4). Our results are similar to other ethnic groups.</p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2017 ","pages":"9427269"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2017/9427269","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34787005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Granulovacuolar Degeneration in Hippocampus of Neurodegenerative Diseases: Quantitative Study","authors":"M. Kurdi, E. Chin, L. Ang","doi":"10.1155/2016/6163186","DOIUrl":"https://doi.org/10.1155/2016/6163186","url":null,"abstract":"Background. Granulovacuolar degeneration (GVD) is one of the pathological features long associated with Alzheimer's disease (AD) and normal aging. Aim. We investigate the frequency of GVDs in AD, other neurodegenerative diseases, and normal aging, with attempt to determine whether the GVD has preponderance in any particular neurodegenerative disease other than AD. Materials and Methods. A retrospective review of 111 autopsied cases with a variety of neurodegenerative diseases and 70 control cases without pathological evidence of neurodegeneration was evaluated quantitatively. The microscopic examination was applied on coronal sections of hippocampi using Hematoxylin and Eosin (H&E) and Bielschowsky silver impregnation. The mean percentage of neurons with GVDs was calculated through all sectors of Ammon's horn for each case. Result. We found that neurons with GVD, in cases with or without neurodegenerative diseases, were found predominantly in CA1 and CA2 sectors of hippocampus. The GVD count in AD was significantly increased in CA1 and CA2 compared to other neurodegenerative cases as well as normal aging controls. In AD/LBD there was a significant increase in GVD in CA1 whereas in LBD there was no significant change in GVD. Conclusions. The frequency of GVD in AD is due to the disease process and attributes the increase for AD/LBD to the AD component.","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73583777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk of Parkinson's Disease in the Users of Antihypertensive Agents: An Evidence from the Meta-Analysis of Observational Studies.","authors":"Amarnath Mullapudi,&nbsp;Kapil Gudala,&nbsp;Chandra Sekhar Boya,&nbsp;Dipika Bansal","doi":"10.1155/2016/5780809","DOIUrl":"https://doi.org/10.1155/2016/5780809","url":null,"abstract":"<p><p>Background. Antihypertensive agents have been shown to inhibit oxidative stress and inflammatory response and thus neuroprotection in Parkinson's disease (PD). Epidemiological evidence suggests inconsistency between use of antihypertensives and risk of PD. This study is aimed to examine the association between antihypertensive use and risk of PD. Methods. Literature search in PubMed, EMBASE, and PsycINFO database was undertaken through February 2012 looking for observational studies evaluating the association between antihypertensive drug use and risk of PD. Before meta-analysis, the studies were evaluated for publication bias and heterogeneity. Pooled relative risk (RR) estimates and 95% confidence intervals (CIs) were calculated using random-effects model (DerSimonian and Laird method). Subgroup analyses and sensitivity analysis were also performed. Results. Seven relevant studies including a total of 28,32,991 subjects were included. Pooled RR of overall use of antihypertensive agents was found to be 0.95 (95% CI 0.84-1.05). A significant reduction in the risk of PD was observed among users of calcium channel blockers (RR 0.82, 95% CI 0.71-0.93). Significant heterogeneity (I (2) = 76.2%) but no publication bias was observed. Conclusions. Overall use of antihypertensive agents showed no significant association with the risk of PD. CCBs provided significant protective role. However, studies with large sample size and dose relationships are required to strengthen our hypothesis. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2016 ","pages":"5780809"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/5780809","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34750909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Intrabody Drug (rAAV6-INT41) Reduces the Binding of N-Terminal Huntingtin Fragment(s) to DNA to Basal Levels in PC12 Cells and Delays Cognitive Loss in the R6/2 Animal Model.","authors":"I Alexandra Amaro,&nbsp;Lee A Henderson","doi":"10.1155/2016/7120753","DOIUrl":"https://doi.org/10.1155/2016/7120753","url":null,"abstract":"<p><p>Huntington's disease (HD) is a fatal progressive disease linked to expansion of glutamine repeats in the huntingtin protein and characterized by the progressive loss of cognitive and motor function. We show that expression of a mutant human huntingtin exon-1-GFP fusion construct results in nonspecific gene dysregulation that is significantly reduced by 50% due to coexpression of INT41, an intrabody specific for the proline-rich region of the huntingtin protein. Using stable PC12 cell lines expressing either inducible human mutant huntingtin (mHtt, Q73) or normal huntingtin (nHtt, Q23), we investigated the effect of rAAV6-INT41, an adeno-associated virus vector with the INT41 coding sequence, on the subcellular distribution of Htt. Compartmental fractionation 8 days after induction of Htt showed a 6-fold increased association of a dominate N-terminal mHtt fragment with DNA compared to N-terminal nHtt. Transduction with rAAV6-INT41 reduced DNA binding of N-terminal mHtt 6.5-fold in the nucleus and reduced nuclear translocation of the detected fragments. Subsequently, when rAAV6-INT41 is delivered to the striatum in the R6/2 mouse model, treated female mice exhibited executive function statistically indistinguishable from wild type, accompanied by reductions in Htt aggregates in the striatum, suggesting that rAAV6-INT41 is promising as a gene therapy for Huntington's disease. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2016 ","pages":"7120753"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2016/7120753","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34417625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valproic Acid Neuroprotection in the 6-OHDA Model of Parkinson's Disease Is Possibly Related to Its Anti-Inflammatory and HDAC Inhibitory Properties.","authors":"José Christian Machado Ximenes,&nbsp;Kelly Rose Tavares Neves,&nbsp;Luzia Kalyne A M Leal,&nbsp;Marta Regina Santos do Carmo,&nbsp;Gerly Anne de Castro Brito,&nbsp;Maria da Graça Naffah-Mazzacoratti,&nbsp;Ésper Abrão Cavalheiro,&nbsp;Glauce Socorro de Barros Viana","doi":"10.1155/2015/313702","DOIUrl":"https://doi.org/10.1155/2015/313702","url":null,"abstract":"<p><p>Parkinson's disease is a neurodegenerative disorder where the main hallmark is the dopaminergic neuronal loss. Besides motor symptoms, PD also causes cognitive decline. Although current therapies focus on the restoration of dopamine levels in the striatum, prevention or disease-modifying therapies are urgently needed. Valproic acid (VA) is a wide spectrum antiepileptic drug, exerting many biochemical and physiological effects. It has been shown to inhibit histone deacetylase which seems to be associated with the drug neuroprotective action. The objectives were to study the neuroprotective properties of VA in a model of Parkinson's disease, consisting in the unilateral striatal injection of the neurotoxin 6-OHDA. For that, male Wistar rats (250 g) were divided into the groups: sham-operated (SO), untreated 6-OHDA-lesioned, and 6-OHDA-lesioned treated with VA (25 or 50 mg/kg). Oral treatments started 24 h after the stereotaxic surgery and continued daily for 2 weeks, when the animals were subjected to behavioral evaluations (apomorphine-induced rotations and open-field tests). Then, they were sacrificed and had their mesencephalon, striatum, and hippocampus dissected for neurochemical (DA and DOPAC determinations), histological (Fluoro-Jade staining), and immunohistochemistry evaluations (TH, OX-42, GFAP, TNF-alpha, and HDAC). The results showed that VA partly reversed behavioral and neurochemical alterations observed in the untreated 6-OHDA-lesioned rats. Besides, VA also decreased neuron degeneration in the striatum and reversed the TH depletion observed in the mesencephalon of the untreated 6-OHDA groups. This neurotoxin increased the OX-42 and GFAP immunoreactivities in the mesencephalon, indicating increased microglia and astrocyte reactivities, respectively, which were reversed by VA. In addition, the immunostainings for TNF-alpha and HDAC demonstrated in the untreated 6-OHDA-lesioned rats were also decreased after VA treatments. These results were observed not only in the CA1 and CA3 subfields of the hippocampus, but also in the temporal cortex. In conclusion, we showed that VA partly reversed the behavioral, neurochemical, histological, and immunohistochemical alterations observed in the untreated 6-OHDA-lesioned animals. These effects are probably related to the drug anti-inflammatory activity and strongly suggest that VA is a potential candidate to be included in translational studies for the treatment of neurodegenerative diseases as PD. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2015 ","pages":"313702"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/313702","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34026652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Essential Tremor in the Elderly and Risk for Dementia.","authors":"Holly A Shill,&nbsp;Joseph G Hentz,&nbsp;Sandra A Jacobson,&nbsp;Christine Belden,&nbsp;Marwan N Sabbagh,&nbsp;Thomas G Beach,&nbsp;Erika Driver-Dunckley,&nbsp;Charles H Adler","doi":"10.1155/2014/328765","DOIUrl":"https://doi.org/10.1155/2014/328765","url":null,"abstract":"<p><p>The objective is to examine the risk of dementia in subjects with essential tremor (ET) involved in the Arizona Study of Aging and Neurodegenerative Disorders. All subjects were free of a neurodegenerative diagnosis at baseline and had annual motor, general neurological, and neuropsychological assessments. Subjects with ET were compared with controls for the risk of dementia. There were 83 subjects with ET and 424 subjects without tremor. Mean age at study entry was 80 ± 5.9 for ET and 76 ± 8.5 for controls. Median tremor duration was 5.2 years at study entry. Followup was a median of 5.4 years (range 0.9 to 12.1). The hazard ratio for the association between ET and dementia was 0.79 (95% CI 0.33 to 1.85). The hazard ratio for the association between tremor onset at age 65 or over, versus onset before age 65, was 2.1 (95% CI 0.24 to 18) and the hazard ratio for the association between tremor duration greater than 5 years, versus less than 5 years, was 0.46 (95% CI 0.08 to 2.6). We conclude that all elderly ET was not associated with an increased risk of dementia but that a subset of subjects with older age onset/shorter duration tremor may be at higher risk. </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2014 ","pages":"328765"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/328765","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34129123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on \"Prevalence and Cognitive Bases of Subjective Memory Complaints in Older Adults: Evidence from a Community Sample\".","authors":"Ashima Nehra,&nbsp;Sakshi Chopra,&nbsp;Harsimarpreet Kaur","doi":"10.1155/2014/240215","DOIUrl":"https://doi.org/10.1155/2014/240215","url":null,"abstract":"It was a pleasure reading your paper entitled “Prevalence and Cognitive Bases of Subjective Memory Complaints in Older Adults: Evidence from a Community Sample,” which was published on 27 April 2014. It was a very detailed paper about the incidence of subjective memory complaints (SMCs) in older adults and how importantly SMCs could have a prognostic value in predicting objective memory decline and dementia [1, 2]. \u0000 \u0000It was very interesting to note the process of making subjects as a part of the study, who are drawn from memory clinics, biased in finding a higher prevalence of SMC as subjects are more likely to have memory impairments, whereas, on the other hand, how population based studies may be biased in finding a lower prevalence of SMC's as the subjects are more willing to participate in research and are also healthier than the patient groups (subjects drawn from memory clinics). \u0000 \u0000However, in the methodology, the clear inclusion and exclusion criteria were not mentioned for the subjects who were made a part of the study. There was no mention about any comorbid conditions or disorders as well, which the participants who were included in the study had, as this information can be important for further having any correlations between the existing comorbid conditions/disorders and SMCs. Also, the subjects were divided into two groups, younger adults and older adults, but there was no mention on what criteria this was based. According to the World Health Organization, any person who is 60 years old and above can be called an elderly or an older population [3], so we would like to know why subjects who were 60 years old and above were not included and why 65 years old and above subjects were enrolled. \u0000 \u0000Moreover, in the methods, there were 3 hypotheses of the study, but there was no mention about them being accepted or rejected. The third objective which stated that gender and objective memory would be associated with a greater risk for SMCs in women than in men was rejected after obtaining the results. The same could have been stated in the results and conclusions. \u0000 \u0000The paper was also very comprehensive about the data and results, but nothing was mentioned about the subjects who actually performed low in the objective neuropsychological evaluation, who turned out to have dementia, whether they referred to a neurology clinic after that for any treatment/intervention or not. The future directions and implications of the study could have been highlighted and how the study can be benefitted to the general population to make substantial generalizations would further strengthen the research. \u0000 \u0000Overall, it was a very interesting study, and we hope that these can be done in India as well, soon.","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2014 ","pages":"240215"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/240215","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34129122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glial Cell Line-Derived Neurotrophic Factor Family Members Reduce Microglial Activation via Inhibiting p38MAPKs-Mediated Inflammatory Responses.","authors":"Uta Rickert,&nbsp;Steffen Grampp,&nbsp;Henrik Wilms,&nbsp;Jessica Spreu,&nbsp;Friederike Knerlich-Lukoschus,&nbsp;Janka Held-Feindt,&nbsp;Ralph Lucius","doi":"10.1155/2014/369468","DOIUrl":"https://doi.org/10.1155/2014/369468","url":null,"abstract":"<p><p>Previous studies have shown that glial cell line-derived neurotrophic factor (GDNF) family ligands (GFL) are potent survival factors for dopaminergic neurons and motoneurons with therapeutic potential for Parkinson's disease. However, little is known about direct influences of the GFL on microglia function, which are known to express part of the GDNF receptor system. Using RT-PCR and immunohistochemistrym we investigated the expression of the GDNF family receptor alpha 1 (GFR alpha) and the coreceptor transmembrane receptor tyrosine kinase (RET) in rat microglia in vitro as well as the effect of GFL on the expression of proinflammatory molecules in LPS activated microglia. We could show that GFL are able to regulate microglia functions and suggest that part of the well known neuroprotective action may be related to the suppression of microglial activation. We further elucidated the functional significance and pathophysiological implications of these findings and demonstrate that microglia are target cells of members of the GFL (GDNF and the structurally related neurotrophic factors neurturin (NRTN), artemin (ARTN), and persephin (PSPN)). </p>","PeriodicalId":16405,"journal":{"name":"Journal of Neurodegenerative Diseases","volume":"2014 ","pages":"369468"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/369468","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34026649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}