کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8456044 | 1548372 | 2010 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Activated astroglia during chronic inflammation in Alzheimer's disease-Do they neglect their neurosupportive roles?
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Activated astroglia during chronic inflammation in Alzheimer's disease-Do they neglect their neurosupportive roles? Activated astroglia during chronic inflammation in Alzheimer's disease-Do they neglect their neurosupportive roles?](/preview/png/8456044.png)
چکیده انگلیسی
Alzheimer's disease (AD) is a neurodegenerative disorder, characterized histopathologically by the extracellular deposition of β-amyloid peptide in senile plaques, as well as intracellular neurofibrillary tangles (NFT) of hyperphosphorylated tau protein, extensive neuronal loss and synaptic changes in the hippocampus and cerebral cortex. In addition, the AD brain shows chronic inflammation characterized by an abundance of reactive astrocytes and activated microglia. In the healthy brain, astrocytes provide essential services for brain homeostasis and neuronal function, including metabolic support for neurons in the form of lactate, glutamate uptake and conversion into glutamine, and synthesis of glutathione and its precursors. In AD, a large body of evidence now suggests that by transforming from a basal to a reactive state, astrocytes neglect their neurosupportive functions, thus rendering neurons vulnerable to neurotoxins including pro-inflammatory cytokines and reactive oxygen species. This review will explain the normal functions of astrocytes, and how these cells might be activated to turn into inflammatory cells, actively contributing to neurodegeneration and neglecting their neurosupportive roles (“neuro-neglect hypothesis”). Furthermore, it is proposed that astrocytes might be promising target of therapeutic intervention for Alzheimer's disease, if these compromised functions can be normalized with pharmacological agents that are specifically designed to return astrocytes to a quiescent phenotype or supplement factors which activated astrocytes lack to produce.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 690, Issues 1â2, 7 August 2010, Pages 40-49
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 690, Issues 1â2, 7 August 2010, Pages 40-49
نویسندگان
Stacey Fuller, Megan Steele, Gerald Münch,