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Sökning: L773:2162 3279 OR L773:2162 3279 > Forskningsöversikt

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1.
  • Aniszewska, Agata, et al. (författare)
  • Modeling Parkinson's disease-related symptoms in alpha-synuclein overexpressing mice
  • 2022
  • Ingår i: Brain and Behavior. - : John Wiley & Sons. - 2162-3279 .- 2162-3279. ; 12:7
  • Forskningsöversikt (refereegranskat)abstract
    • Background: Intracellular deposition of alpha-synuclein (alpha-syn) as Lewy bodies and Lewy neurites is a central event in the pathogenesis of Parkinson's disease (PD) and other alpha-synucleinopathies. Transgenic mouse models overexpressing human alpha-syn, are useful research tools in preclinical studies of pathogenetic mechanisms. Such mice develop alpha-syn inclusions as well as neurodegeneration with a topographical distribution that varies depending on the choice of promoter and which form of alpha-syn that is overexpressed. Moreover, they display motor symptoms and cognitive disturbances that to some extent resemble the human conditions.Purpose: One of the main motives for assessing behavior in these mouse models is to evaluate the potential of new treatment strategies, including their impact on motor and cognitive symptoms. However, due to a high within-group variability with respect to such features, the behavioral studies need to be applied with caution. In this review, we discuss how to make appropriate choices in the experimental design and which tests that are most suitable for the evaluation of PD-related symptoms in such studies.Methods: We have evaluated published results on two selected transgenic mouse models overexpressing wild type (L61) and mutated (A30P) alpha-syn in the context of their validity and utility for different types of behavioral studies.Conclusions: By applying appropriate behavioral tests, alpha-syn transgenic mouse models provide an appropriate experimental platform for studies of symptoms related to PD and other alpha-synucleinopathies.
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2.
  • Cedergren Weber, Gustav, et al. (författare)
  • Tumoral parkinsonism—Parkinsonism secondary to brain tumors, paraneoplastic syndromes, intracranial malformations, or oncological intervention, and the effect of dopaminergic treatment
  • 2023
  • Ingår i: Brain and Behavior. - 2162-3279. ; 13:8
  • Forskningsöversikt (refereegranskat)abstract
    • Introduction: Secondary tumoral parkinsonism is a rare phenomenon that develops as a direct or indirect result of brain neoplasms or related conditions. Objectives: The first objective was to explore to what extent brain neoplasms, cavernomas, cysts, paraneoplastic syndromes (PNSs), and oncological treatment methods cause parkinsonism. The second objective was to investigate the effect of dopaminergic therapy on the symptomatology in patients with tumoral parkinsonism. Methods: A systematic literature review was conducted in the databases PubMed and Embase. Search terms like “secondary parkinsonism,” “astrocytoma,” and “cranial irradiation” were used. Articles fulfilling inclusion criteria were included in the review. Results: Out of 316 identified articles from the defined database search strategies, 56 were included in the detailed review. The studies, which were mostly case reports, provided research concerning tumoral parkinsonism and related conditions. It was found that various types of primary brain tumors, such as astrocytoma and meningioma, and more seldom brain metastases, can cause tumoral parkinsonism. Parkinsonism secondary to PNSs, cavernomas, cysts, as well as oncological treatments was reported. Twenty-five of the 56 included studies had tried initiating dopaminergic therapy, and of these 44% reported no, 48% low to moderate, and 8% excellent effect on motor symptomatology. Conclusion: Brain neoplasms, PNSs, certain intracranial malformations, and oncological treatments can cause parkinsonism. Dopaminergic therapy has relatively benign side effects and may relieve motor and nonmotor symptomatology in patients with tumoral parkinsonism. Dopaminergic therapy, particularly levodopa, should therefore be considered in patients with tumoral parkinsonism.
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3.
  • Ferreira, Luiz Kobuti, et al. (författare)
  • Functional connectivity in behavioral variant frontotemporal dementia
  • 2022
  • Ingår i: Brain and Behavior. - : Wiley. - 2162-3279. ; 12:12
  • Forskningsöversikt (refereegranskat)abstract
    • Introduction: Functional connectivity (FC)—which reflects relationships between neural activity in different brain regions—has been used to explore the functional architecture of the brain in neurodegenerative disorders. Although an increasing number of studies have explored FC changes in behavioral variant frontotemporal dementia (bvFTD), there is no focused, in-depth review about FC in bvFTD. Methods: Comprehensive literature search and narrative review to summarize the current field of FC in bvFTD. Results: (1) Decreased FC within the salience network (SN) is the most consistent finding in bvFTD; (2) FC changes extend beyond the SN and affect the interplay between networks; (3) results within the Default Mode Network are mixed; (4) the brain as a network is less interconnected and less efficient in bvFTD; (5) symptoms, functional impairment, and cognition are associated with FC; and (6) the functional architecture resembles patterns of neuropathological spread. Conclusions: FC has potential as a biomarker, and future studies are expected to advance the field with multicentric initiatives, longitudinal designs, and methodological advances.
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4.
  • Shah, Syed Muhammad Ismail, et al. (författare)
  • COVID‐19 and myasthenia gravis : A review of neurological implications of the SARS‐COV‐2
  • 2022
  • Ingår i: Brain and Behavior. - : Wiley. - 2162-3279 .- 2162-3279. ; 12:12
  • Forskningsöversikt (refereegranskat)abstract
    • IntroductionThis review highlights the potential mechanisms of neuromuscular manifestation of COVID-19, especially myasthenia gravis (MG).MethodsAn extensive literature search was conducted by two independent investigators using PubMed/MEDLINE and Google Scholar from its inception to December 2020.ResultsExacerbations of clinical symptoms in patients of MG who were treated with some commonly used COVID-19 drugs has been reported, with updated recommendations of management of symptoms of neuromuscular disorders. Severe acute respiratory syndrome coronavirus 2 can induce the immune response to trigger autoimmune neurological disorders.ConclusionsFurther clinical studies are warranted to indicate and rather confirm if MG in the setting of COVID-19 can pre-existent subclinically or develop as a new-onset disease.
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