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      Introduction to the recommendations from the National Institute on Aging‐Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

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          Abstract

          Criteria for the clinical diagnosis of Alzheimer's disease (AD) were established in 1984. A broad consensus now exists that these criteria should be revised to incorporate state-of-the-art scientific knowledge. The National Institute on Aging (NIA) and the Alzheimer's Association sponsored a series of advisory round table meetings in 2009 whose purpose was to establish a process for revising diagnostic and research criteria for AD. The recommendation from these advisory meetings was that three separate work groups should be formed with each assigned the task of formulating diagnostic criteria for one phase of the disease: the dementia phase; the symptomatic, pre-dementia phase; and the asymptomatic, preclinical phase of AD. Two notable differences from the AD criteria published in 1984 are incorporation of biomarkers of the underlying disease state and formalization of different stages of disease in the diagnostic criteria. There was a broad consensus within all three workgroups that much additional work is needed to validate the application of biomarkers for diagnostic purposes. In the revised NIA-Alzheimer's Association criteria, a semantic and conceptual distinction is made between AD pathophysiological processes and clinically observable syndromes that result, whereas this distinction was blurred in the 1984 criteria. The new criteria for AD are presented in three documents. The core clinical criteria of the recommendations regarding AD dementia and MCI due to AD are intended to guide diagnosis in the clinical setting. However, the recommendations of the preclinical AD workgroup are intended purely for research purposes. Copyright © 2011 The Alzheimer's Association. All rights reserved.

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          Most cited references50

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              The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

              It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.
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                Author and article information

                Journal
                Alzheimer's & Dementia
                Alzheimer's & Dementia
                Elsevier BV
                1552-5260
                1552-5279
                May 2011
                April 22 2011
                May 2011
                : 7
                : 3
                : 257-262
                Affiliations
                [1 ]Department of Radiology Mayo ClinicRochesterMNUSA
                [2 ]Department of NeurologyJohns Hopkins University School of MedicineBaltimoreMDUSA
                [3 ]Center for Alzheimer Research and Treatment, Brigham and Women's Hosptial, Massachusetts General Hospital Harvard Medical SchoolBostonMAUSA
                [4 ]Alzheimer's AssociationChicagoILUSA
                [5 ]Division of NeuroscieneNational Institute on AgingBethesdaMDUSA
                Article
                10.1016/j.jalz.2011.03.004
                3096735
                21514247
                23f67f76-cadb-47c3-9329-d74e42c57b40
                © 2011

                http://onlinelibrary.wiley.com/termsAndConditions#vor

                http://doi.wiley.com/10.1002/tdm_license_1.1

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