کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5716009 | 1411128 | 2016 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The neuropathology of neurodegenerative diseases causing dementia
ترجمه فارسی عنوان
نوروپاتولوژی بیماری های عصبی ناشی از زوال عقل
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کلمات کلیدی
chronic traumatic encephalopathy - انسفالوپاتی مزمن ترومایتیAlzheimer's disease - بیماری آلزایمرDementia - جنون یا زوال عقلfrontotemporal lobar degeneration - دژنراسیون لوبار قبل از مواجههDLB, Dementia with Lewy bodies - زوال عقل با اجسام لوییfrontotemporal dementia - فراموشی پیشانی گیجگاهی، انحطاط پیشانی گیجگاهی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
آسیبشناسی و فناوری پزشکی
چکیده انگلیسی
The dementia syndrome is increasing in prevalence throughout the developed world as the population ages. For example, in the United States it is estimated that between 2000 and 2020, the number of people living to 100 years or more will increase by over 200%, and the number of people surviving to 90-95 years will double. Based on these and other epidemiologic data, the prevalence of diseases causing the dementia syndrome has and will continue to increase dramatically over the next several decades. Considering Alzheimer's disease alone, the most common cause of dementia in the elderly, there are currently 5.5 million persons affected in the United States, and that prevalence will increase to 16 million by the first half of this century. This review will focus on the histopathology of important neurodegenerative diseases of the brain that cause dementia, including Alzheimer's disease, frontotemporal lobar degenerations, and dementia with Lewy bodies. In addition, a less common but extraordinarily interesting condition, chronic traumatic encephalopathy, will be reviewed.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Diagnostic Histopathology - Volume 22, Issue 11, November 2016, Pages 424-430
Journal: Diagnostic Histopathology - Volume 22, Issue 11, November 2016, Pages 424-430
نویسندگان
William W. Pendlebury,