کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
7280444 | 1473913 | 2016 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cognitive deficits develop 1Â month after diffuse brain injury and are exaggerated by microglia-associated reactivity to peripheral immune challenge
ترجمه فارسی عنوان
نقص شناختی یک ماه پس از آسیب مغزی منتشر ایجاد می شود و با واکنش پذیری میکروگلاییا به چالش های ایمنی محیطی بیش از حد افزایش می یابد
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
چکیده انگلیسی
Traumatic brain injury (TBI) is a major risk factor in development of neuropsychiatric problems long after injury, negatively affecting quality of life. Mounting evidence indicates that inflammatory processes worsen with time after a brain injury and are likely mediated by glia. Here, we show that primed microglia and astrocytes developed in mice 1Â month following moderate diffuse TBI, coinciding with cognitive deficits that were not initially evident after injury. Additionally, TBI-induced glial priming may adversely affect the ability of glia to appropriately respond to immune challenges, which occur regularly across the lifespan. Indeed, we show that an acute immune challenge augmented microglial reactivity and cognitive deficits. This idea may provide new avenues of clinical assessments and treatments following TBI.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain, Behavior, and Immunity - Volume 54, May 2016, Pages 95-109
Journal: Brain, Behavior, and Immunity - Volume 54, May 2016, Pages 95-109
نویسندگان
Megan M. Muccigrosso, Joni Ford, Brooke Benner, Daniel Moussa, Christopher Burnsides, Ashley M. Fenn, Phillip G. Popovich, Jonathan Lifshitz, Fredrick Rohan Walker, Daniel S. Eiferman, Jonathan P. Godbout,