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Sökning: L773:0885 3185

  • Resultat 21-30 av 345
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21.
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22.
  • Bezard, Erwan, et al. (författare)
  • Animal Models of Parkinson's Disease: Limits and Relevance to Neuroprotection Studies
  • 2013
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 28:1, s. 61-70
  • Forskningsöversikt (refereegranskat)abstract
    • Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology and pathogenesis of Parkinson's disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modeling PD revolves around what can be called the disease gene-based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine-producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease-related genes. In this position article, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that, we argue, should be utilized in the preclinical development phase of new neuroprotective therapies before embarking into clinical trials. (C) 2012 Movement Disorder Society
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23.
  • Bezard, Erwan, et al. (författare)
  • Study of the antidyskinetic effect of eltoprazine in animal models of levodopa-induced dyskinesia
  • 2013
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 28:8, s. 1088-1096
  • Tidskriftsartikel (refereegranskat)abstract
    • The serotonin (5-hydroxytryptamine [5HT]) system has recently emerged as an important player in the appearance of l-3,4-dihydroxyphenylalanine (levodopa [l-dopa])-induced dyskinesia in animal models of Parkinson's disease. In fact, dopamine released as a false transmitter from serotonin neurons appears to contribute to the pulsatile stimulation of dopamine receptors, leading to the appearance of the abnormal involuntary movements. Thus, drugs able to dampen the activity of serotonin neurons hold promise for the treatment of dyskinesia. The authors investigated the ability of the mixed 5-HT 1A/1B receptor agonist eltoprazine to counteract l-dopa-induced dyskinesia in 6-hydroxydopamine-lesioned rats and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated macaques. The data demonstrated that eltoprazine is extremely effective in suppressing dyskinesia in experimental models, although this effect was accompanied by a partial worsening of the therapeutic effect of l-dopa. Interestingly, eltoprazine was found to (synergistically) potentiate the antidyskinetic effect of amantadine. The current data indicated that eltoprazine is highly effective in counteracting dyskinesia in preclinical models. However, the partial worsening of the l-dopa effect observed after eltoprazine administration represents a concern; whether this side effect is due to a limitation of the animal models or to an intrinsic property of eltoprazine needs to be addressed in ongoing clinical trials. The data also suggest that the combination of low doses of eltoprazine with amantadine may represent a valid strategy to increase the antidyskinetic effect and reduce the eltoprazine-induced worsening of l-dopa therapeutic effects. (c) 2013 Movement Disorder Society
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24.
  • Björklund, Anders, et al. (författare)
  • Cell therapy for Parkinson's disease: what next?
  • 2013
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 28:1, s. 110-115
  • Tidskriftsartikel (refereegranskat)abstract
    • The idea to use transplants of dopamine-producing cells to substitute for the lost midbrain dopamine neurons in Parkinson's disease (PD) goes back to the 1970s. In this review we give an overview of the history of cell transplantation in animal models of PD, and summarize the experience gained from the open-label and placebo-controlled clinical trials performed so far using intrastriatal transplants of human fetal dopamine neuroblasts. Further development of this therapeutic approach face numerous challenges, for example in the development of protocols that allow generation of fully functional and safe midbrain dopamine neurons from stem cells. Based on recent promising advancements, efforts are now being made to develop standardized and efficient protocols, and adapt these protocols to good laboratory practice (GLP)/good manufacturing practice (GMP) conditions, to move this technology closer to clinical translation. © 2013 Movement Disorder Society.
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25.
  • Björklund, Tomas, et al. (författare)
  • Gene therapy for Parkinson's disease.
  • 2010
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 25 Suppl 1, s. 161-173
  • Tidskriftsartikel (refereegranskat)abstract
    • The once fantastic theoretical concept that patients with Parkinson's disease (PD) would receive gene therapy in an attempt to alleviate their symptoms and potentially modify the course of their disease has become a reality. On the basis of positive preclinical data, four different gene therapy approaches are currently in Phase I or Phase II clinical trials. Some approaches are intended to increase levels of endogenous dopamine or enhance the function of the prodrug levodopa. Others are intended to normalize basal ganglia circuitry by reducing the PD-related overactivity of specific brain structures such as the subthalamic nucleus. Each is intended for symptomatic benefit. Finally, gene delivery of trophic factors that not only augment dopaminergic function but are potentially disease modifying has a strong preclinical database and are also in clinical trials. Each of these approaches is discussed in the present review.
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26.
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27.
  • Blennow, Kaj, 1958, et al. (författare)
  • Cerebrospinal Fluid Biomarkers in Alzheimer's and Parkinson's Diseases-From Pathophysiology to Clinical Practice
  • 2016
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185. ; 31:6, s. 836-847
  • Tidskriftsartikel (refereegranskat)abstract
    • This review provides an update on the role, development, and validation of CSF biomarkers in the diagnosis and prognosis of Alzheimer's disease and PD. Some recent developments on novel biomarkers are also discussed. We also give an overview of methodological/technical factors still hampering the global validation and standardization of CSF Alzheimer's disease and PD biomarkers. CSF biomarkers have the potential to improve the diagnostic accuracy at the early stages not only for Alzheimer's disease but also for PD. This step is essential in view of the availability of disease-modifying treatments. Our vision for the future is that analyzing biomarker panels on a minute amount of CSF could provide important information on the whole spectrum of the molecular pathogenic events characterizing these neurodegenerative disorders. CSF core biomarkers have already been included in the diagnostic criteria for Alzheimer's disease, and they are also under consideration as tools to monitor the effects of disease-modifying drugs. With respect to PD, their potential for improving diagnostic accuracy in early diagnosis is under intense research, resembling the same path followed for Alzheimer's disease.
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28.
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29.
  • Blomstedt, Patric, et al. (författare)
  • A family with a hereditary form of torsion dystonia from northern Sweden treated with bilateral pallidal deep brain stimulation
  • 2009
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185 .- 1531-8257. ; 24:16, s. 2415-2419
  • Tidskriftsartikel (refereegranskat)abstract
    • To evaluate pallidal DBS in a non-DYT1 form of hereditary dystonia. We present the results of pallidal DBS in a family with non-DYT1 dystonia where DYT5 to 17 was excluded. The dystonia is following an autosomal dominant pattern. Ten members had definite dystonia and five had dystonia with minor symptoms. Four patients received bilateral pallidal DBS. Mean age was 47 years. The patients were evaluated before surgery, and "on" stimulation after a mean of 2.5 years (range 1-3) using the Burke-Fahn-Marsden scale (BFM). Mean BFM score decreased by 79 % on stimulation, from 42.5 +/- 24 to 9 +/- 6.5 at the last evaluation. Cervical involvement improved by 89%. The 2 patients with oromandibular dystonia and blepharospasm demonstrated a reduction of 95% regarding these symptoms. The present study confirms the effectiveness of pallidal DBS in a new family with hereditary primary segmental and generalized dystonia.
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30.
  • Blomstedt, Patric, et al. (författare)
  • Deep brain stimulation in the posterior subthalamic area in the treatment of essential tremor
  • 2010
  • Ingår i: Movement Disorders. - : Wiley. - 0885-3185 .- 1531-8257. ; 25:10, s. 1350-1356
  • Tidskriftsartikel (refereegranskat)abstract
    • To evaluate the posterior subthalamic area (PSA) as a target for deep brain stimulation (DBS) in the treatment of essential tremor (ET). The ventral intermediate nucleus of the thalamus is the traditional target for DBS in the treatment of ET. Recent studies have presented beneficial effects of DBS in the PSA in the treatment of tremor. Twenty-one patients with ET were included in this study. All patients were evaluated before and 1 year after surgery, on and off stimulation, using the essential tremor rating scale (ETRS). A marked microlesional effect was noticed in 83%, in some cases obviating the need for electrical stimulation for many months. The total ETRS was reduced from 46.2 at baseline to 18.7 (60%). Item 5/6 (tremor of the upper extremity) was improved from 6.2 to 0.3 (95%), and items 11 to 14 (hand function) from 9.7 to 1.3 (87%) concerning the contralateral hand. Activities of daily living were improved by 66%. No severe complication occurred. Eight patients presented a postoperative mild dysphasia that regressed within days to weeks. DBS in the PSA resulted in a marked reduction of tremor.
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