کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8673744 | 1578847 | 2017 | 17 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Alzheimer Disease
ترجمه فارسی عنوان
بیماری آلزایمر
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کلمات کلیدی
CERADPSENConsortium to Establish a Registry for Alzheimer's DiseaseFDATREM2fluorodeoxyglucoseNFTFDGAPPApoe - آپوapolipoprotein E - آپولیپوپروتئین Emild cognitive impairment - اختلال شناختی خفیفMRI - امآرآی یا تصویرسازی تشدید مغناطیسیAlzheimer disease - بیماری آلزایمرMagnetic resonance imaging - تصویربرداری رزونانس مغناطیسیPositron emission tomography - توموگرافی گسیل پوزیترونNeurofibrillary tangle - خلط نوروفیبریلاDIAD - دیادFood and Drug Administration - سازمان غذا و داروREVEAL - فاش کردنCSF - مایع مغزی نخاعیCerebrospinal fluid - مایع مغزی نخاعیMCI - همراه اولPET - پتPresenilin - پرنسیلینamyloid precursor protein - پروتئین پیش ماده آمیلوئیtriggering receptor expressed on myeloid cells 2 - گیرنده ای که به سلول های میلوئید بیان می شود 2 است
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
چکیده انگلیسی
Alzheimer disease (AD) was originally conceived as a rare disease that caused presenile dementia but has come to be understood as the most prevalent cause of dementia at any age worldwide. It has an extended preclinical phase characterized by sequential changes in imaging and cerebrospinal fluid biomarkers with subtle memory decline beginning more than a decade before the emergence of symptomatic memory loss heralding the beginning of the mild cognitive impairment stage. The apolipoprotein E ε4 allele is a prevalent and potent risk factor for AD that has facilitated research into its preclinical phase. Cerebral Aβ levels build from preclinical through early dementia stages followed by hyperphosphorylated tau-related pathology, the latter driving cognitive deficits and dementia severity. Structural and molecular imaging can now recapitulate the neuropathology of AD antemortem. Autosomal dominant forms of early-onset familial AD gave rise to the amyloid hypothesis of AD, which, in turn, has led to therapeutic trials of immunotherapy designed to clear cerebral amyloid, but to date results have been disappointing. Genome-wide association studies have identified multiple additional risk factors, but to date none have yielded an effective alternate therapeutic target. Current and future trials aimed at presymptomatic individuals either harboring cerebral amyloid or at genetically high risk offer the hope that earlier intervention might yet succeed where trials in patients with established dementia have failed. A major looming challenge will be that of expensive, incompletely effective disease-modifying therapy: who and when to treat, and how to pay for it.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mayo Clinic Proceedings - Volume 92, Issue 6, June 2017, Pages 978-994
Journal: Mayo Clinic Proceedings - Volume 92, Issue 6, June 2017, Pages 978-994
نویسندگان
Richard J. MD, Thomas G. MD, PhD, David S. MD, Neill R. MD,