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Assessing the Feasibility of Adipose-derived Stem Cells to Alleviate Neurodegeneration in MSA Animal Models

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Patients with multiple system atrophy (MSA), a progressive neurodegenerative disorder of adult onset, were found less than 9-year life expectancy after onset. The disorders include bradykinesia and rigidity commonly seen in Parkinsonism disease and additional signs such as autonomic dysfunction, at

axia, or dementia. MSA-P, representing 80% of MSA, is characterized by striatonigral neurodegeneration (SND) where parkinsonism predominates. In clinical treatments, MSA poorly responds to levodopa, the drug used to remedy Parkinsonism disease. The exact cause of MSA is still unknown and exploring a

therapeutic solution to MSA remains critical. The potential of stem cell therapy for neural degenerative diseases has been widely explored recently. With the reported abilities to differentiate into neuronal linage and to secrete neurotrophic factors for neuronal support, mesenchymal stem cells (MS

C) presents a possible therapeutic option for MSA-P. Among the sources of MSC, adipose-derived stem cells (ADSC) are relatively easier to obtain and less invasive. To conduct the feasibility study in vivo, toxin-based MSA-P mouse model and transgenic MSA mouse model were established. Toxin-based mod

el, chemically (3NP + MPTP) inducing MSA-P in C57BL/6N mice, was established to assess the effect of ADSC on improving motion behavior of MSA-P mouse. Molecular mechanism was investigated using transgenic MSA mouse model to reveal the role of ADSC in alleviating neurodegeneration of MBP1 mouse. MBP1

transgenic mice, transferred from the University of California in San Diego, USA (UCSD), have been reported in studying α-synuclein associated neurodegeneration. Our transgenic mouse model established from MBP1 mouse provides a useful tool to investigate the effect of ADSC on the biomarker for MSA,

i.e., α-synuclein glial cytoplasmic inclusion (GCI) in oligodendrocytes. Human ADSC were transplanted into the striatum of MSA animals via intracerebral injection (IC). Testing intranasal (INA) delivery route was withdrawn due to brain blood barrier (BBB) issue. The grafted ADSC was traced by label

ing ADSC with transduced GFP and taking photo images on live mice. The presence of ADSC was detected from immunofluorescence (IF) stains 4 weeks post grafting. The alleviation of neurodegeneration after ADSC treatment was indicated by improved performance in animal behavior testing, including rotaro

d test and pole test. As compared with a sham control, ADSC significantly enhanced Rotarod performance of MSA animals treated with ADSC at an effective dose (2x10^5 ADSC/mouse). Our ex vivo study supported that ADSC might alleviate striatal degeneration in MSA animal model by improving nigrostriatal

pathway for dopamine, activating autophagy for α-synuclein clearance, decreasing inflammatory signal and further cell apoptosis, improving myelination and cell survival at caudate-putamen. Mitochondria was found to transfer from ADSC to injured neuron in vitro. ADSC pretreated with mitochondria-ric

h chemical (MR1) had beneficial trend in improving Rotarod performance although the difference against ADSC was not statistically significant.