کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6803760 | 1433549 | 2015 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Thrombospondin-1 prevents amyloid beta-mediated synaptic pathology in Alzheimer's disease
ترجمه فارسی عنوان
ترومبوسپوندن-1 مانع آسیب شناسی سیناپسی توسط آمیلوئید بتا در بیماری آلزایمر می شود
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Alzheimer's disease (AD) is characterized by impaired cognitive function and memory loss, which are often the result of synaptic pathology. Thrombospondin (TSP) is an astrocyte-secreted protein, well known for its function as a modulator of synaptogenesis and neurogenesis. Here, we investigated the effects of TSP-1 on AD pathogenesis. We found that the level of TSP-1 expression was decreased in AD brains. When we treated astrocytes with amyloid beta (Aβ), secreted TSP-1 was decreased in autophagy-dependent manner. In addition, treatment with Aβ induced synaptic pathology, such as decreased dendritic spine density and reduced synaptic activity. These effects were prevented by coincubation of TSP-1 with Aβ, which acts through the TSP-1 receptor alpha-2-delta-1 in neurons. Finally, intrasubicular injection with TSP-1 into AD model mouse brains mitigated the Aβ-mediated reduction of synaptic proteins and related signaling pathways. These results indicate that TSP-1 is a potential therapeutic target in AD pathogenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 36, Issue 12, December 2015, Pages 3214-3227
Journal: Neurobiology of Aging - Volume 36, Issue 12, December 2015, Pages 3214-3227
نویسندگان
Sung Min Son, Dong Woo Nam, Moon-Yong Cha, Kyung Ho Kim, Jayoung Byun, Hoon Ryu, Inhee Mook-Jung,