کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9192011 | 1186610 | 2005 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tau phosphorylation increases in symptomatic mice overexpressing A30P α-synuclein
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
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چکیده انگلیسی
Mice overexpressing mutant α-synuclein develop a progressive loss of motor function associated with the accumulation of aggregated α-synuclein in neurons of the brainstem. Recent reports suggest that tau pathology might also be associated with Parkinson disease (PD) and aggregation of α-synuclein. We now report that mice overexpressing A30P α-synuclein develop abnormally phosphorylated tau in parallel with the accumulation of aggregated α-synuclein. Enhanced phosphorylation of tau occurs only in symptomatic mice that also harbor abundant aggregated α-synuclein. The increased phosphorylation of tau occurs at S396/404 and S202 as shown by immunoblotting and immunocytochemical studies with the antibodies PHF-1 and AT8. Neurons that accumulated α-synuclein occurred in the dorsal brainstem and did not show strong colocalization with neurons that showed abnormal tau phosphorylation, which largely occurred in the ventral brainstem. Aggregation of α-synuclein and phosphorylation of tau are associated with increased levels of phosphorylated c-jun kinase (JNK), which is a stress kinase known to phosphorylate tau protein. These results suggest that α-synuclein pathology can stimulate early pathological changes in tau.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 192, Issue 2, April 2005, Pages 274-287
Journal: Experimental Neurology - Volume 192, Issue 2, April 2005, Pages 274-287
نویسندگان
M. Frasier, M. Walzer, L. McCarthy, D. Magnuson, J.M. Lee, C. Haas, P. Kahle, B. Wolozin,