Tau positron emission tomographic imaging in aging and early Alzheimer disease
Objective Detection of focal brain tau deposition during life could greatly facilitate accurate diagnosis of Alzheimer disease (AD), staging and monitoring of disease progression, and development of disease‐modifying therapies. Methods We acquired tau positron emission tomography (PET) using 18F T80...
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| Veröffentlicht in: | Annals of neurology 2016-01, Vol.79 (1), p.110-119 |
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| container_title | Annals of neurology |
| container_volume | 79 |
| creator | Johnson, Keith A. Schultz, Aaron Betensky, Rebecca A. Becker, J. Alex Sepulcre, Jorge Rentz, Dorene Mormino, Elizabeth Chhatwal, Jasmeer Amariglio, Rebecca Papp, Kate Marshall, Gad Albers, Mark Mauro, Samantha Pepin, Lesley Alverio, Jonathan Judge, Kelly Philiossaint, Marlie Shoup, Timothy Yokell, Daniel Dickerson, Bradford Gomez-Isla, Teresa Hyman, Bradley Vasdev, Neil Sperling, Reisa |
| description | Objective
Detection of focal brain tau deposition during life could greatly facilitate accurate diagnosis of Alzheimer disease (AD), staging and monitoring of disease progression, and development of disease‐modifying therapies.
Methods
We acquired tau positron emission tomography (PET) using 18F T807 (AV1451), and amyloid‐β PET using 11C Pittsburgh compound B (PiB) in older clinically normal individuals, and symptomatic patients with mild cognitive impairment or mild AD dementia.
Results
We found abnormally high cortical 18F T807 binding in patients with mild cognitive impairment and AD dementia compared to clinically normal controls. Consistent with the neuropathology literature, the presence of elevated neocortical 18F T807 binding particularly in the inferior temporal gyrus was associated with clinical impairment. The association of cognitive impairment was stronger with inferior temporal 18F T807 than with mean cortical 11C PIB. Regional 18F T807 was correlated with mean cortical 11C PiB among both impaired and control subjects.
Interpretation
These findings suggest that 18F T807 PET could have value as a biomarker that reflects both the progression of AD tauopathy and the emergence of clinical impairment. ANN NEUROL 2016;79:110–119 |
| doi_str_mv | 10.1002/ana.24546 |
| format | Article |
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Detection of focal brain tau deposition during life could greatly facilitate accurate diagnosis of Alzheimer disease (AD), staging and monitoring of disease progression, and development of disease‐modifying therapies.
Methods
We acquired tau positron emission tomography (PET) using 18F T807 (AV1451), and amyloid‐β PET using 11C Pittsburgh compound B (PiB) in older clinically normal individuals, and symptomatic patients with mild cognitive impairment or mild AD dementia.
Results
We found abnormally high cortical 18F T807 binding in patients with mild cognitive impairment and AD dementia compared to clinically normal controls. Consistent with the neuropathology literature, the presence of elevated neocortical 18F T807 binding particularly in the inferior temporal gyrus was associated with clinical impairment. The association of cognitive impairment was stronger with inferior temporal 18F T807 than with mean cortical 11C PIB. Regional 18F T807 was correlated with mean cortical 11C PiB among both impaired and control subjects.
Interpretation
These findings suggest that 18F T807 PET could have value as a biomarker that reflects both the progression of AD tauopathy and the emergence of clinical impairment. ANN NEUROL 2016;79:110–119</description><identifier>ISSN: 0364-5134</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.24546</identifier><identifier>PMID: 26505746</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Aged ; Aged, 80 and over ; Aging - metabolism ; Alzheimer Disease - metabolism ; Alzheimer Disease - physiopathology ; Amyloid beta-Peptides - metabolism ; Aniline Compounds ; Biomarkers - metabolism ; Carbolines - metabolism ; Cerebral Cortex - metabolism ; Cognitive ability ; Cognitive Dysfunction - metabolism ; Cognitive Dysfunction - physiopathology ; Dementia ; Female ; Humans ; Male ; Middle Aged ; Positron-Emission Tomography - methods ; tau Proteins - metabolism ; Temporal Lobe - metabolism ; Thiazoles</subject><ispartof>Annals of neurology, 2016-01, Vol.79 (1), p.110-119</ispartof><rights>2015 American Neurological Association</rights><rights>2015 American Neurological Association.</rights><rights>2016 American Neurological Association</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fana.24546$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fana.24546$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26505746$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Johnson, Keith A.</creatorcontrib><creatorcontrib>Schultz, Aaron</creatorcontrib><creatorcontrib>Betensky, Rebecca A.</creatorcontrib><creatorcontrib>Becker, J. Alex</creatorcontrib><creatorcontrib>Sepulcre, Jorge</creatorcontrib><creatorcontrib>Rentz, Dorene</creatorcontrib><creatorcontrib>Mormino, Elizabeth</creatorcontrib><creatorcontrib>Chhatwal, Jasmeer</creatorcontrib><creatorcontrib>Amariglio, Rebecca</creatorcontrib><creatorcontrib>Papp, Kate</creatorcontrib><creatorcontrib>Marshall, Gad</creatorcontrib><creatorcontrib>Albers, Mark</creatorcontrib><creatorcontrib>Mauro, Samantha</creatorcontrib><creatorcontrib>Pepin, Lesley</creatorcontrib><creatorcontrib>Alverio, Jonathan</creatorcontrib><creatorcontrib>Judge, Kelly</creatorcontrib><creatorcontrib>Philiossaint, Marlie</creatorcontrib><creatorcontrib>Shoup, Timothy</creatorcontrib><creatorcontrib>Yokell, Daniel</creatorcontrib><creatorcontrib>Dickerson, Bradford</creatorcontrib><creatorcontrib>Gomez-Isla, Teresa</creatorcontrib><creatorcontrib>Hyman, Bradley</creatorcontrib><creatorcontrib>Vasdev, Neil</creatorcontrib><creatorcontrib>Sperling, Reisa</creatorcontrib><title>Tau positron emission tomographic imaging in aging and early Alzheimer disease</title><title>Annals of neurology</title><addtitle>Ann Neurol</addtitle><description>Objective
Detection of focal brain tau deposition during life could greatly facilitate accurate diagnosis of Alzheimer disease (AD), staging and monitoring of disease progression, and development of disease‐modifying therapies.
Methods
We acquired tau positron emission tomography (PET) using 18F T807 (AV1451), and amyloid‐β PET using 11C Pittsburgh compound B (PiB) in older clinically normal individuals, and symptomatic patients with mild cognitive impairment or mild AD dementia.
Results
We found abnormally high cortical 18F T807 binding in patients with mild cognitive impairment and AD dementia compared to clinically normal controls. Consistent with the neuropathology literature, the presence of elevated neocortical 18F T807 binding particularly in the inferior temporal gyrus was associated with clinical impairment. The association of cognitive impairment was stronger with inferior temporal 18F T807 than with mean cortical 11C PIB. Regional 18F T807 was correlated with mean cortical 11C PiB among both impaired and control subjects.
Interpretation
These findings suggest that 18F T807 PET could have value as a biomarker that reflects both the progression of AD tauopathy and the emergence of clinical impairment. ANN NEUROL 2016;79:110–119</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging - metabolism</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Aniline Compounds</subject><subject>Biomarkers - metabolism</subject><subject>Carbolines - metabolism</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cognitive ability</subject><subject>Cognitive Dysfunction - metabolism</subject><subject>Cognitive Dysfunction - physiopathology</subject><subject>Dementia</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Positron-Emission Tomography - methods</subject><subject>tau Proteins - metabolism</subject><subject>Temporal Lobe - metabolism</subject><subject>Thiazoles</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkTlP7DAUhS3EEwxLwR9AkWhoAt6dlCOWAQkNBSAkGusmuRkMWQZ7Ihh-PYbhUVBR3SPd73g5h5A9Ro8YpfwYOjjiUkm9RkZMCZZmXObrZESFlqliQm6SrRCeKKW5ZnSDbHKtqDJSj8j0FoZk3ge38H2XYOtCcFEs-rafeZg_ujJxLcxcN0tcl6wEdFWC4JtlMm7eH9G16JPKBYSAO-RfDU3A3e-5Te7Oz25PLtKr68nlyfgqdYoznULBJK80FAUFURihBNJMQpUjlgLKogIUJlNYI8U65zIreSENrytVV0LoXGyTw9W5c9-_DBgWNr68xKaBDvshWGaM1lIxLf-Aai6k0hmP6MEv9KkffBc_EillMsOU-bx7_5saihYrO_cxIb-0_0ONwPEKeHUNLn_2jNrPtmxsy361ZcfT8ZeIjnTlcGGBbz8O8M9WG2GUvZ9ObD65fzi_uTi1UnwAEpCVdw</recordid><startdate>201601</startdate><enddate>201601</enddate><creator>Johnson, Keith A.</creator><creator>Schultz, Aaron</creator><creator>Betensky, Rebecca A.</creator><creator>Becker, J. Alex</creator><creator>Sepulcre, Jorge</creator><creator>Rentz, Dorene</creator><creator>Mormino, Elizabeth</creator><creator>Chhatwal, Jasmeer</creator><creator>Amariglio, Rebecca</creator><creator>Papp, Kate</creator><creator>Marshall, Gad</creator><creator>Albers, Mark</creator><creator>Mauro, Samantha</creator><creator>Pepin, Lesley</creator><creator>Alverio, Jonathan</creator><creator>Judge, Kelly</creator><creator>Philiossaint, Marlie</creator><creator>Shoup, Timothy</creator><creator>Yokell, Daniel</creator><creator>Dickerson, Bradford</creator><creator>Gomez-Isla, Teresa</creator><creator>Hyman, Bradley</creator><creator>Vasdev, Neil</creator><creator>Sperling, Reisa</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201601</creationdate><title>Tau positron emission tomographic imaging in aging and early Alzheimer disease</title><author>Johnson, Keith A. ; Schultz, Aaron ; Betensky, Rebecca A. ; Becker, J. Alex ; Sepulcre, Jorge ; Rentz, Dorene ; Mormino, Elizabeth ; Chhatwal, Jasmeer ; Amariglio, Rebecca ; Papp, Kate ; Marshall, Gad ; Albers, Mark ; Mauro, Samantha ; Pepin, Lesley ; Alverio, Jonathan ; Judge, Kelly ; Philiossaint, Marlie ; Shoup, Timothy ; Yokell, Daniel ; Dickerson, Bradford ; Gomez-Isla, Teresa ; Hyman, Bradley ; Vasdev, Neil ; Sperling, Reisa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i5216-ab142d6abb0a3b7353e084ad9eec3acbdae3785efe0ef9248c2b472fd5fd33693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging - metabolism</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Aniline Compounds</topic><topic>Biomarkers - metabolism</topic><topic>Carbolines - metabolism</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cognitive ability</topic><topic>Cognitive Dysfunction - metabolism</topic><topic>Cognitive Dysfunction - physiopathology</topic><topic>Dementia</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Positron-Emission Tomography - methods</topic><topic>tau Proteins - metabolism</topic><topic>Temporal Lobe - metabolism</topic><topic>Thiazoles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Johnson, Keith A.</creatorcontrib><creatorcontrib>Schultz, Aaron</creatorcontrib><creatorcontrib>Betensky, Rebecca A.</creatorcontrib><creatorcontrib>Becker, J. Alex</creatorcontrib><creatorcontrib>Sepulcre, Jorge</creatorcontrib><creatorcontrib>Rentz, Dorene</creatorcontrib><creatorcontrib>Mormino, Elizabeth</creatorcontrib><creatorcontrib>Chhatwal, Jasmeer</creatorcontrib><creatorcontrib>Amariglio, Rebecca</creatorcontrib><creatorcontrib>Papp, Kate</creatorcontrib><creatorcontrib>Marshall, Gad</creatorcontrib><creatorcontrib>Albers, Mark</creatorcontrib><creatorcontrib>Mauro, Samantha</creatorcontrib><creatorcontrib>Pepin, Lesley</creatorcontrib><creatorcontrib>Alverio, Jonathan</creatorcontrib><creatorcontrib>Judge, Kelly</creatorcontrib><creatorcontrib>Philiossaint, Marlie</creatorcontrib><creatorcontrib>Shoup, Timothy</creatorcontrib><creatorcontrib>Yokell, Daniel</creatorcontrib><creatorcontrib>Dickerson, Bradford</creatorcontrib><creatorcontrib>Gomez-Isla, Teresa</creatorcontrib><creatorcontrib>Hyman, Bradley</creatorcontrib><creatorcontrib>Vasdev, Neil</creatorcontrib><creatorcontrib>Sperling, Reisa</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Johnson, Keith A.</au><au>Schultz, Aaron</au><au>Betensky, Rebecca A.</au><au>Becker, J. Alex</au><au>Sepulcre, Jorge</au><au>Rentz, Dorene</au><au>Mormino, Elizabeth</au><au>Chhatwal, Jasmeer</au><au>Amariglio, Rebecca</au><au>Papp, Kate</au><au>Marshall, Gad</au><au>Albers, Mark</au><au>Mauro, Samantha</au><au>Pepin, Lesley</au><au>Alverio, Jonathan</au><au>Judge, Kelly</au><au>Philiossaint, Marlie</au><au>Shoup, Timothy</au><au>Yokell, Daniel</au><au>Dickerson, Bradford</au><au>Gomez-Isla, Teresa</au><au>Hyman, Bradley</au><au>Vasdev, Neil</au><au>Sperling, Reisa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tau positron emission tomographic imaging in aging and early Alzheimer disease</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>2016-01</date><risdate>2016</risdate><volume>79</volume><issue>1</issue><spage>110</spage><epage>119</epage><pages>110-119</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><abstract>Objective
Detection of focal brain tau deposition during life could greatly facilitate accurate diagnosis of Alzheimer disease (AD), staging and monitoring of disease progression, and development of disease‐modifying therapies.
Methods
We acquired tau positron emission tomography (PET) using 18F T807 (AV1451), and amyloid‐β PET using 11C Pittsburgh compound B (PiB) in older clinically normal individuals, and symptomatic patients with mild cognitive impairment or mild AD dementia.
Results
We found abnormally high cortical 18F T807 binding in patients with mild cognitive impairment and AD dementia compared to clinically normal controls. Consistent with the neuropathology literature, the presence of elevated neocortical 18F T807 binding particularly in the inferior temporal gyrus was associated with clinical impairment. The association of cognitive impairment was stronger with inferior temporal 18F T807 than with mean cortical 11C PIB. Regional 18F T807 was correlated with mean cortical 11C PiB among both impaired and control subjects.
Interpretation
These findings suggest that 18F T807 PET could have value as a biomarker that reflects both the progression of AD tauopathy and the emergence of clinical impairment. ANN NEUROL 2016;79:110–119</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>26505746</pmid><doi>10.1002/ana.24546</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Aged Aged, 80 and over Aging - metabolism Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Amyloid beta-Peptides - metabolism Aniline Compounds Biomarkers - metabolism Carbolines - metabolism Cerebral Cortex - metabolism Cognitive ability Cognitive Dysfunction - metabolism Cognitive Dysfunction - physiopathology Dementia Female Humans Male Middle Aged Positron-Emission Tomography - methods tau Proteins - metabolism Temporal Lobe - metabolism Thiazoles |
| title | Tau positron emission tomographic imaging in aging and early Alzheimer disease |
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