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How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture
A seismic shift in our understanding of the ability to diagnose Alzheimer disease (AD) is occurring. For the last several decades, AD has been a clinical–pathologic diagnosis, and this conceptualization of the disease has served the field well. Typically, the clinician would identify a syndrome such...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Lippincott Williams & Wilkins
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6133623/ https://www.ncbi.nlm.nih.gov/pubmed/30089620 http://dx.doi.org/10.1212/WNL.0000000000006088 |
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author | Petersen, Ronald C. |
author_facet | Petersen, Ronald C. |
author_sort | Petersen, Ronald C. |
collection | PubMed |
description | A seismic shift in our understanding of the ability to diagnose Alzheimer disease (AD) is occurring. For the last several decades, AD has been a clinical–pathologic diagnosis, and this conceptualization of the disease has served the field well. Typically, the clinician would identify a syndrome such as mild cognitive impairment or dementia, and label the condition as “probable AD” since the diagnosis of definite AD could not be made until an autopsy revealed the presence of amyloid plaques and tau-based neurofibrillary tangles. However, with the advent of biomarkers for AD including neuroimaging and CSF, the identification of AD pathology can be made in life, which greatly enhances the ability of clinicians to be precise about the underlying etiology of a clinical syndrome. Hypothetical models of the temporal relation among the pathologic elements and the clinical symptoms have been proposed and have influenced the field enormously. This has enabled clinicians to be specific about the underlying cause of a given clinical syndrome. As such, the diagnostic capability of the clinician is evolving. However, AD pathology is only a component of the puzzle describing the causes of cognitive changes in aging. Most often, there is a multitude of pathologic entities contributing to the neuropathologic explanation of cognitive changes in aging. AD changes contribute important elements to the diagnosis, but the final answer is more complex. The field of aging and dementia will have to incorporate these additional elements. |
format | Online Article Text |
id | pubmed-6133623 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-61336232018-09-12 How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture Petersen, Ronald C. Neurology Special Invited Article A seismic shift in our understanding of the ability to diagnose Alzheimer disease (AD) is occurring. For the last several decades, AD has been a clinical–pathologic diagnosis, and this conceptualization of the disease has served the field well. Typically, the clinician would identify a syndrome such as mild cognitive impairment or dementia, and label the condition as “probable AD” since the diagnosis of definite AD could not be made until an autopsy revealed the presence of amyloid plaques and tau-based neurofibrillary tangles. However, with the advent of biomarkers for AD including neuroimaging and CSF, the identification of AD pathology can be made in life, which greatly enhances the ability of clinicians to be precise about the underlying etiology of a clinical syndrome. Hypothetical models of the temporal relation among the pathologic elements and the clinical symptoms have been proposed and have influenced the field enormously. This has enabled clinicians to be specific about the underlying cause of a given clinical syndrome. As such, the diagnostic capability of the clinician is evolving. However, AD pathology is only a component of the puzzle describing the causes of cognitive changes in aging. Most often, there is a multitude of pathologic entities contributing to the neuropathologic explanation of cognitive changes in aging. AD changes contribute important elements to the diagnosis, but the final answer is more complex. The field of aging and dementia will have to incorporate these additional elements. Lippincott Williams & Wilkins 2018-08-28 /pmc/articles/PMC6133623/ /pubmed/30089620 http://dx.doi.org/10.1212/WNL.0000000000006088 Text en Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND) (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. |
spellingShingle | Special Invited Article Petersen, Ronald C. How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture |
title | How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture |
title_full | How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture |
title_fullStr | How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture |
title_full_unstemmed | How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture |
title_short | How early can we diagnose Alzheimer disease (and is it sufficient)?: The 2017 Wartenberg lecture |
title_sort | how early can we diagnose alzheimer disease (and is it sufficient)?: the 2017 wartenberg lecture |
topic | Special Invited Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6133623/ https://www.ncbi.nlm.nih.gov/pubmed/30089620 http://dx.doi.org/10.1212/WNL.0000000000006088 |
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