کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6806927 | 1433577 | 2013 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Aβ increases neural stem cell activity in senescence-accelerated SAMP8 mice
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Neurogenesis persists in the adult brain as a form of plasticity due to the existence of neural stem cells (NSCs). Alterations in neurogenesis have been found in transgenic Alzheimer's disease (AD) mouse models, but NSC activity and neurogenesis in sporadic AD models remains to be examined. We herein describe a remarkable increase in NSC proliferation in the forebrain of SAMP8, a non-transgenic mouse strain that recapitulates the transition from healthy aging to AD. The increase in proliferation is transient, precedes AD-like symptoms such as amyloid beta 1-42 [Aβ(1-42)] increase or gliosis, and is followed by a steep decline at later stages. Interestingly, in vitro studies indicate that secreted Aβ(1-42) and PI3K signaling may account for the early boost in NSC proliferation. Our results highlight the role of soluble Aβ(1-42) peptide and PI3K in the autocrine regulation of NSCs, and further suggest that over-proliferation of NSCs before the appearance of AD pathology may underlie neurogenic failure during the age-related progression of the disease. These findings have implications for therapeutic approaches based on neurogenesis in AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 34, Issue 11, November 2013, Pages 2623-2638
Journal: Neurobiology of Aging - Volume 34, Issue 11, November 2013, Pages 2623-2638
نویسندگان
MarÃa DÃaz-Moreno, Rafael Hortigüela, Ania Gonçalves, Irmina GarcÃa-Carpio, Gemma Manich, Edurne GarcÃa-Bermúdez, Mireia Moreno-Estellés, César Eguiluz, Jordi Vilaplana, Carme PelegrÃ, Marçal Vilar, Helena Mira,