کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
7280358 | 1473912 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Microglia in dementia with Lewy bodies
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کلمات کلیدی
Non-dementedNFDDLBNeuroinflammation - التهاب عصبیLewy body - بدن لویAlzheimer’s disease - بیماری آلزایمرNeurodegenerative disease - بیماری های نوروژنیکParkinson’s disease - بیماری پارکینسونDementia with Lewy bodies - تهوع و استفراغ با بدن LewyCNS - دستگاه عصبی مرکزیNeurofibrillary degeneration - دژنراسیون نوروفیبریلیالcentral nervous system - سیستم عصبی مرکزیLewy neurites - عصبهای Lewymicroglial activation - فعال سازی microglialLipofuscin - لیپوفوسینmajor histocompatibility complex - مجموعه سازگاری بافتی اصلیMHC - مجموعه سازگاری بافتی اصلی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Microglial activation (neuroinflammation) is often cited as a pathogenic factor in the development of neurodegenerative diseases. However, there are significant caveats associated with the idea that inflammation directly causes either α-synuclein pathology or neurofibrillary degeneration (NFD). We have performed immunohistochemical studies on microglial cells in five cases of dementia with Lewy bodies (DLB), median age 87, and nine cases of non-demented (ND) controls, median age 74, using tissue samples from the temporal lobe and the superior frontal gyrus. Three different antibodies known to label microglia and macrophages were employed: iba1, anti-CD68, and anti-ferritin. All DLB cases showed both α-synuclein pathology (Lewy bodies and neurites) and NFD ranging from Braak stage II to IV. In contrast, all controls were devoid of α-synuclein pathology but did show NFD ranging from Braak stage I to III. Using iba1 labeling, our current results show a notable absence of activated microglia in all cases with the exception of two controls that showed small focal areas of microglial activation and macrophage formation. Both iba1 and ferritin antibodies revealed a mixture of ramified and dystrophic microglial cells throughout the regions examined, and there were no measurable differences in the prevalence of dystrophic microglial cells between DLB and controls. Double-labeling for α-synuclein and iba1-positive microglia showed that cortical Lewy bodies were surrounded by both ramified and dystrophic microglial cells. We found an increase in CD68 expression in DLB cases relative to controls. Since microglial dystrophy has been linked to NFD and since it did not appear to be worse in DLB cases over controls, our findings support the idea that the additional Lewy body pathology in DLB is not the result of intensified microglial dystrophy. CD68 is likely associated with lipofuscin deposits in microglial cells which may be increased in DLB cases because of impaired proteostasis. Overall, we conclude that neurodegenerative changes in DLB are unlikely to result directly from activated microglia but rather from dysfunctional ones.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain, Behavior, and Immunity - Volume 55, July 2016, Pages 191-201
Journal: Brain, Behavior, and Immunity - Volume 55, July 2016, Pages 191-201
نویسندگان
Wolfgang J. Streit, Qing-Shan Xue,