کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9191904 | 1186604 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ethyl-EPA treatment improves motor dysfunction, but not neurodegeneration in the YAC128 mouse model of Huntington disease
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کلمات کلیدی
UHDRSEPAPBSRPMDARPP-32Motor dysfunction - اختلال در عملکرد موتورEicosapentaenoic acid - اسید ایکوزاپنتانوئیکEssential fatty acid - اسید چرب ضروریHuntington disease - بیماری هانتینگتونanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاNeurodegeneration - تولید نوروژنیکstandard error of the mean - خطای استاندارد میانگینexperimental therapeutics - درمان های تجربیrevolutions per minute - سرعت در هر دقیقهPhosphate buffered saline - فسفات بافر شورSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیTransgenic mouse model - مدل موش ترانسژنیک
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Ethyl-EPA treatment improves motor dysfunction, but not neurodegeneration in the YAC128 mouse model of Huntington disease Ethyl-EPA treatment improves motor dysfunction, but not neurodegeneration in the YAC128 mouse model of Huntington disease](/preview/png/9191904.png)
چکیده انگلیسی
Huntington disease (HD) is an adult-onset neurodegenerative disorder that is characterized by selective degeneration in the striatum. There are currently no treatments that can prevent the progressive decline of motor and cognitive function in HD. In parallel with a human clinical trial, we examined the efficacy of ethyl-EPA treatment in the YAC128 mouse model of HD. Oral delivery of ethyl-EPA to symptomatic YAC128 mice beginning at 7 months of age increased membrane EPA levels 3-fold (PÂ <Â 0.001) and resulted in a modest but significant improvement in motor dysfunction by 12 months of age as measured by open-field activity (PÂ =Â 0.01) and performance on the rotarod (PÂ =Â 0.05). At this age, ethyl-EPA-treated YAC128 mice showed no improvement in striatal volume, striatal neuron counts, striatal neuronal cross-sectional area, or striatal DARPP-32 expression compared to untreated YAC128 mice, thereby indicating no reduction of striatal neuropathology. This result is congruent with modest motor benefits observed in HD patients treated with ethyl-EPA. Overall, this work demonstrates the feasibility of experimental therapeutics in the YAC128 mouse model and suggests that experiments in these mice may be predictive for future human clinical trials.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 196, Issue 2, December 2005, Pages 266-272
Journal: Experimental Neurology - Volume 196, Issue 2, December 2005, Pages 266-272
نویسندگان
Jeremy M. Van Raamsdonk, Jacqueline Pearson, Daniel A. Rogers, Ge Lu, Vilte E. Barakauskas, Alasdair M. Barr, William G. Honer, Michael R. Hayden, Blair R. Leavitt,