PET imaging of brain amyloid in dementia: a review
Identifieur interne : 002752 ( Main/Corpus ); précédent : 002751; suivant : 002753PET imaging of brain amyloid in dementia: a review
Auteurs : Harriet Quigley ; Sean J. Colloby ; John T. O'BrienSource :
- International Journal of Geriatric Psychiatry [ 0885-6230 ] ; 2011-10.
English descriptors
Abstract
Objective: To review the rapidly expanding literature of amyloid PET imaging with particular attention to Pittsburgh compound‐B (PIB) in Alzheimer's disease (AD), dementia with Lewy bodies (DLB), fronto‐temporal dementia (FTD), mild cognitive impairment (MCI) and cognitively normal volunteers. Design: Literature searches were performed using Medline up to February 2010. Individual articles were then examined for additional references not revealed by automated searches. This yielded 79 articles whose abstracts were read by the authors to select key papers. Results: Amyloid deposition assessed using PIB‐PET is significantly elevated in AD and DLB compared to controls and those with FTD. In MCI, uptake is often intermediate between AD and normal ageing, and excessive amyloid burden in non‐demented individuals with MCI are likely to represent high‐risk cases. Amyloid deposition appears to be an early event, and as dementia progresses clinical decline seems to be more associated with neurodegeneration than amyloid burden. Conclusions: PIB‐PET imaging is a sensitive and specific marker for underlying Aβ amyloid deposition and represents an important investigative tool for examining the relationship between amyloid burden, clinical symptoms and structural and functional changes in dementia. Amyloid imaging may also be useful for selecting patients for anti‐amyloid therapies. However, studies have identified PIB‐positive cases in otherwise healthy older individuals (10–30%), limiting diagnostic specificity. Development of biomarkers for investigating other aspects of dementia pathology, i.e. soluble Aβ, tau, synuclein and brain inflammation would further inform our understanding and assist in studying disease‐modifying and preventive treatments in dementia. Copyright © 2010 John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/gps.2640
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ISTEX:3A0A8481AFD553AF1B7605E520401949AC8760D5Le document en format XML
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Design: Literature searches were performed using Medline up to February 2010. Individual articles were then examined for additional references not revealed by automated searches. This yielded 79 articles whose abstracts were read by the authors to select key papers. Results: Amyloid deposition assessed using PIB‐PET is significantly elevated in AD and DLB compared to controls and those with FTD. In MCI, uptake is often intermediate between AD and normal ageing, and excessive amyloid burden in non‐demented individuals with MCI are likely to represent high‐risk cases. Amyloid deposition appears to be an early event, and as dementia progresses clinical decline seems to be more associated with neurodegeneration than amyloid burden. Conclusions: PIB‐PET imaging is a sensitive and specific marker for underlying Aβ amyloid deposition and represents an important investigative tool for examining the relationship between amyloid burden, clinical symptoms and structural and functional changes in dementia. Amyloid imaging may also be useful for selecting patients for anti‐amyloid therapies. However, studies have identified PIB‐positive cases in otherwise healthy older individuals (10–30%), limiting diagnostic specificity. Development of biomarkers for investigating other aspects of dementia pathology, i.e. soluble Aβ, tau, synuclein and brain inflammation would further inform our understanding and assist in studying disease‐modifying and preventive treatments in dementia. Copyright © 2010 John Wiley & Sons, Ltd.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Harriet Quigley</name><affiliations><json:string>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK</json:string></affiliations></json:item><json:item><name>Sean J. Colloby</name><affiliations><json:string>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK</json:string></affiliations></json:item><json:item><name>John T. O'Brien</name><affiliations><json:string>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>amyloid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MCI</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ageing</value></json:item></subject><articleId><json:string>GPS2640</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objective: To review the rapidly expanding literature of amyloid PET imaging with particular attention to Pittsburgh compound‐B (PIB) in Alzheimer's disease (AD), dementia with Lewy bodies (DLB), fronto‐temporal dementia (FTD), mild cognitive impairment (MCI) and cognitively normal volunteers. Design: Literature searches were performed using Medline up to February 2010. Individual articles were then examined for additional references not revealed by automated searches. This yielded 79 articles whose abstracts were read by the authors to select key papers. Results: Amyloid deposition assessed using PIB‐PET is significantly elevated in AD and DLB compared to controls and those with FTD. In MCI, uptake is often intermediate between AD and normal ageing, and excessive amyloid burden in non‐demented individuals with MCI are likely to represent high‐risk cases. Amyloid deposition appears to be an early event, and as dementia progresses clinical decline seems to be more associated with neurodegeneration than amyloid burden. Conclusions: PIB‐PET imaging is a sensitive and specific marker for underlying Aβ amyloid deposition and represents an important investigative tool for examining the relationship between amyloid burden, clinical symptoms and structural and functional changes in dementia. Amyloid imaging may also be useful for selecting patients for anti‐amyloid therapies. However, studies have identified PIB‐positive cases in otherwise healthy older individuals (10–30%), limiting diagnostic specificity. Development of biomarkers for investigating other aspects of dementia pathology, i.e. soluble Aβ, tau, synuclein and brain inflammation would further inform our understanding and assist in studying disease‐modifying and preventive treatments in dementia. 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Design: Literature searches were performed using Medline up to February 2010. Individual articles were then examined for additional references not revealed by automated searches. This yielded 79 articles whose abstracts were read by the authors to select key papers. Results: Amyloid deposition assessed using PIB‐PET is significantly elevated in AD and DLB compared to controls and those with FTD. In MCI, uptake is often intermediate between AD and normal ageing, and excessive amyloid burden in non‐demented individuals with MCI are likely to represent high‐risk cases. Amyloid deposition appears to be an early event, and as dementia progresses clinical decline seems to be more associated with neurodegeneration than amyloid burden. Conclusions: PIB‐PET imaging is a sensitive and specific marker for underlying Aβ amyloid deposition and represents an important investigative tool for examining the relationship between amyloid burden, clinical symptoms and structural and functional changes in dementia. Amyloid imaging may also be useful for selecting patients for anti‐amyloid therapies. However, studies have identified PIB‐positive cases in otherwise healthy older individuals (10–30%), limiting diagnostic specificity. Development of biomarkers for investigating other aspects of dementia pathology, i.e. soluble Aβ, tau, synuclein and brain inflammation would further inform our understanding and assist in studying disease‐modifying and preventive treatments in dementia. 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Individual articles were then examined for additional references not revealed by automated searches. This yielded 79 articles whose abstracts were read by the authors to select key papers.</p></section><section xml:id="abs1-3"><title type="main">Results</title><p>Amyloid deposition assessed using PIB‐PET is significantly elevated in AD and DLB compared to controls and those with FTD. In MCI, uptake is often intermediate between AD and normal ageing, and excessive amyloid burden in non‐demented individuals with MCI are likely to represent high‐risk cases. Amyloid deposition appears to be an early event, and as dementia progresses clinical decline seems to be more associated with neurodegeneration than amyloid burden.</p></section><section xml:id="abs1-4"><title type="main">Conclusions</title><p>PIB‐PET imaging is a sensitive and specific marker for underlying Aβ amyloid deposition and represents an important investigative tool for examining the relationship between amyloid burden, clinical symptoms and structural and functional changes in dementia. Amyloid imaging may also be useful for selecting patients for anti‐amyloid therapies. However, studies have identified PIB‐positive cases in otherwise healthy older individuals (10–30%), limiting diagnostic specificity. Development of biomarkers for investigating other aspects of dementia pathology, i.e. soluble Aβ, tau, synuclein and brain inflammation would further inform our understanding and assist in studying disease‐modifying and preventive treatments in dementia. 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Design: Literature searches were performed using Medline up to February 2010. Individual articles were then examined for additional references not revealed by automated searches. This yielded 79 articles whose abstracts were read by the authors to select key papers. Results: Amyloid deposition assessed using PIB‐PET is significantly elevated in AD and DLB compared to controls and those with FTD. In MCI, uptake is often intermediate between AD and normal ageing, and excessive amyloid burden in non‐demented individuals with MCI are likely to represent high‐risk cases. Amyloid deposition appears to be an early event, and as dementia progresses clinical decline seems to be more associated with neurodegeneration than amyloid burden. Conclusions: PIB‐PET imaging is a sensitive and specific marker for underlying Aβ amyloid deposition and represents an important investigative tool for examining the relationship between amyloid burden, clinical symptoms and structural and functional changes in dementia. Amyloid imaging may also be useful for selecting patients for anti‐amyloid therapies. However, studies have identified PIB‐positive cases in otherwise healthy older individuals (10–30%), limiting diagnostic specificity. Development of biomarkers for investigating other aspects of dementia pathology, i.e. soluble Aβ, tau, synuclein and brain inflammation would further inform our understanding and assist in studying disease‐modifying and preventive treatments in dementia. 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