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Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?
Purpose Posterior cingulate cortex (PCC) hypometabolism as measured by FDG PET is an indicator of Alzheimer’s disease (AD) in prodromal stages, such as in mild cognitive impairment (MCI), and has been found to be closely associated with hippocampus atrophy in AD dementia. We studied the effects of l...
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| Published in: | European journal of nuclear medicine and molecular imaging 2016-03, Vol.43 (3), p.526-536 |
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| cited_by | cdi_FETCH-LOGICAL-c639t-551d363b47ae0fbb50ef29e8a1ba879487f294b604e5354ff2676398a8b9d1a73 |
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| cites | cdi_FETCH-LOGICAL-c639t-551d363b47ae0fbb50ef29e8a1ba879487f294b604e5354ff2676398a8b9d1a73 |
| container_end_page | 536 |
| container_issue | 3 |
| container_start_page | 526 |
| container_title | European journal of nuclear medicine and molecular imaging |
| container_volume | 43 |
| creator | Teipel, Stefan Grothe, Michel J. |
| description | Purpose
Posterior cingulate cortex (PCC) hypometabolism as measured by FDG PET is an indicator of Alzheimer’s disease (AD) in prodromal stages, such as in mild cognitive impairment (MCI), and has been found to be closely associated with hippocampus atrophy in AD dementia. We studied the effects of local and remote atrophy and of local amyloid load on the PCC metabolic signal in patients with different preclinical and clinical stages of AD.
Methods
We determined the volume of the hippocampus and PCC grey matter based on volumetric MRI scans, PCC amyloid load based on AV45 PET, and PCC metabolism based on FDG PET in 667 subjects participating in the Alzheimer’s Disease Neuroimaging Initiative spanning the range from cognitively normal ageing through prodromal AD to AD dementia.
Results
In cognitively normal individuals and those with early MCI, PCC hypometabolism was exclusively associated with hippocampus atrophy, whereas in subjects with late MCI it was associated with both local and remote effects of atrophy as well as local amyloid load. In subjects with AD dementia, PCC hypometabolism was exclusively related to local atrophy.
Conclusion
Our findings suggest that the effects of remote pathology on PCC hypometabolism decrease and the effects of local pathology increase from preclinical to clinical stages of AD, consistent with a progressive disconnection of the PCC from downstream cortical and subcortical brain regions. |
| doi_str_mv | 10.1007/s00259-015-3222-3 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6166099</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3936188891</sourcerecordid><originalsourceid>FETCH-LOGICAL-c639t-551d363b47ae0fbb50ef29e8a1ba879487f294b604e5354ff2676398a8b9d1a73</originalsourceid><addsrcrecordid>eNqNkstu1TAQhiMEoqXwAGyQJTZsAr7Etw2oKlepEhtYW04yyXHl2MFOKh1WfYkueD2eBJ-eclSQkFjZo_n-f-zRX1VPCX5JMJavMsaU6xoTXjNKac3uVcdEEF1LrPT9w13io-pRzhcYE0WVflgdUcE5x4oeV9dvI2Q0x7xAcjGhzoVx9XYBtNnOcYLFttG7PKEEefULGlKcUO9yF0OAbnExoKLysbMezXbZRB_HLbJdirnYJui8C27XtKFHhyIvdixj44BO_fcNuAnSz6sfeWcMNsObx9WDwfoMT27Pk-rr-3dfzj7W558_fDo7Pa87wfRSc056JljbSAt4aFuOYaAalCWtVVI3SpayaQVugDPeDAMVsgiVVa3uiZXspHq9953XdoK-g7Ak682c3GTT1kTrzJ-d4DZmjJdGECGw1sXgxa1Bit9WyIuZym7AexsgrtkQKbiWZSr_H5Q0EjOlCvr8L_QirimUTdxQuCFM4EKRPXWz7ATD4d0Em10-zD4fpuTD7PJhWNE8u_vhg-J3IApA90AurTBCujP6n66_AJo0ynM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1761041360</pqid></control><display><type>article</type><title>Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?</title><source>Springer Nature:Jisc Collections:Springer Nature Read and Publish 2023-2025: Springer Reading List</source><creator>Teipel, Stefan ; Grothe, Michel J.</creator><creatorcontrib>Teipel, Stefan ; Grothe, Michel J. ; Alzheimer´s Disease Neuroimaging Initiative ; for the Alzheimer´s Disease Neuroimaging Initiative</creatorcontrib><description>Purpose
Posterior cingulate cortex (PCC) hypometabolism as measured by FDG PET is an indicator of Alzheimer’s disease (AD) in prodromal stages, such as in mild cognitive impairment (MCI), and has been found to be closely associated with hippocampus atrophy in AD dementia. We studied the effects of local and remote atrophy and of local amyloid load on the PCC metabolic signal in patients with different preclinical and clinical stages of AD.
Methods
We determined the volume of the hippocampus and PCC grey matter based on volumetric MRI scans, PCC amyloid load based on AV45 PET, and PCC metabolism based on FDG PET in 667 subjects participating in the Alzheimer’s Disease Neuroimaging Initiative spanning the range from cognitively normal ageing through prodromal AD to AD dementia.
Results
In cognitively normal individuals and those with early MCI, PCC hypometabolism was exclusively associated with hippocampus atrophy, whereas in subjects with late MCI it was associated with both local and remote effects of atrophy as well as local amyloid load. In subjects with AD dementia, PCC hypometabolism was exclusively related to local atrophy.
Conclusion
Our findings suggest that the effects of remote pathology on PCC hypometabolism decrease and the effects of local pathology increase from preclinical to clinical stages of AD, consistent with a progressive disconnection of the PCC from downstream cortical and subcortical brain regions.</description><identifier>ISSN: 1619-7070</identifier><identifier>EISSN: 1619-7089</identifier><identifier>DOI: 10.1007/s00259-015-3222-3</identifier><identifier>PMID: 26555082</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Aged ; Aging ; Alzheimer Disease - diagnostic imaging ; Alzheimer Disease - metabolism ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Atrophy ; Cardiology ; Cognition ; Cognitive Dysfunction - diagnostic imaging ; Cognitive Dysfunction - metabolism ; Cognitive Dysfunction - physiopathology ; Female ; Fluorodeoxyglucose F18 - chemistry ; Gray Matter - diagnostic imaging ; Gray Matter - pathology ; Gyrus Cinguli - metabolism ; Gyrus Cinguli - physiopathology ; Hippocampus - diagnostic imaging ; Hippocampus - pathology ; Humans ; Image Processing, Computer-Assisted ; Imaging ; Magnetic Resonance Imaging ; Male ; Medical diagnosis ; Medicine ; Medicine & Public Health ; Metabolism ; Middle Aged ; Nuclear Medicine ; Oncology ; Original Article ; Orthopedics ; Pathology ; Positron-Emission Tomography ; Radiology</subject><ispartof>European journal of nuclear medicine and molecular imaging, 2016-03, Vol.43 (3), p.526-536</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c639t-551d363b47ae0fbb50ef29e8a1ba879487f294b604e5354ff2676398a8b9d1a73</citedby><cites>FETCH-LOGICAL-c639t-551d363b47ae0fbb50ef29e8a1ba879487f294b604e5354ff2676398a8b9d1a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26555082$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Teipel, Stefan</creatorcontrib><creatorcontrib>Grothe, Michel J.</creatorcontrib><creatorcontrib>Alzheimer´s Disease Neuroimaging Initiative</creatorcontrib><creatorcontrib>for the Alzheimer´s Disease Neuroimaging Initiative</creatorcontrib><title>Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?</title><title>European journal of nuclear medicine and molecular imaging</title><addtitle>Eur J Nucl Med Mol Imaging</addtitle><addtitle>Eur J Nucl Med Mol Imaging</addtitle><description>Purpose
Posterior cingulate cortex (PCC) hypometabolism as measured by FDG PET is an indicator of Alzheimer’s disease (AD) in prodromal stages, such as in mild cognitive impairment (MCI), and has been found to be closely associated with hippocampus atrophy in AD dementia. We studied the effects of local and remote atrophy and of local amyloid load on the PCC metabolic signal in patients with different preclinical and clinical stages of AD.
Methods
We determined the volume of the hippocampus and PCC grey matter based on volumetric MRI scans, PCC amyloid load based on AV45 PET, and PCC metabolism based on FDG PET in 667 subjects participating in the Alzheimer’s Disease Neuroimaging Initiative spanning the range from cognitively normal ageing through prodromal AD to AD dementia.
Results
In cognitively normal individuals and those with early MCI, PCC hypometabolism was exclusively associated with hippocampus atrophy, whereas in subjects with late MCI it was associated with both local and remote effects of atrophy as well as local amyloid load. In subjects with AD dementia, PCC hypometabolism was exclusively related to local atrophy.
Conclusion
Our findings suggest that the effects of remote pathology on PCC hypometabolism decrease and the effects of local pathology increase from preclinical to clinical stages of AD, consistent with a progressive disconnection of the PCC from downstream cortical and subcortical brain regions.</description><subject>Aged</subject><subject>Aging</subject><subject>Alzheimer Disease - diagnostic imaging</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Atrophy</subject><subject>Cardiology</subject><subject>Cognition</subject><subject>Cognitive Dysfunction - diagnostic imaging</subject><subject>Cognitive Dysfunction - metabolism</subject><subject>Cognitive Dysfunction - physiopathology</subject><subject>Female</subject><subject>Fluorodeoxyglucose F18 - chemistry</subject><subject>Gray Matter - diagnostic imaging</subject><subject>Gray Matter - pathology</subject><subject>Gyrus Cinguli - metabolism</subject><subject>Gyrus Cinguli - physiopathology</subject><subject>Hippocampus - diagnostic imaging</subject><subject>Hippocampus - pathology</subject><subject>Humans</subject><subject>Image Processing, Computer-Assisted</subject><subject>Imaging</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medical diagnosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Nuclear Medicine</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Pathology</subject><subject>Positron-Emission Tomography</subject><subject>Radiology</subject><issn>1619-7070</issn><issn>1619-7089</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkstu1TAQhiMEoqXwAGyQJTZsAr7Etw2oKlepEhtYW04yyXHl2MFOKh1WfYkueD2eBJ-eclSQkFjZo_n-f-zRX1VPCX5JMJavMsaU6xoTXjNKac3uVcdEEF1LrPT9w13io-pRzhcYE0WVflgdUcE5x4oeV9dvI2Q0x7xAcjGhzoVx9XYBtNnOcYLFttG7PKEEefULGlKcUO9yF0OAbnExoKLysbMezXbZRB_HLbJdirnYJui8C27XtKFHhyIvdixj44BO_fcNuAnSz6sfeWcMNsObx9WDwfoMT27Pk-rr-3dfzj7W558_fDo7Pa87wfRSc056JljbSAt4aFuOYaAalCWtVVI3SpayaQVugDPeDAMVsgiVVa3uiZXspHq9953XdoK-g7Ak682c3GTT1kTrzJ-d4DZmjJdGECGw1sXgxa1Bit9WyIuZym7AexsgrtkQKbiWZSr_H5Q0EjOlCvr8L_QirimUTdxQuCFM4EKRPXWz7ATD4d0Em10-zD4fpuTD7PJhWNE8u_vhg-J3IApA90AurTBCujP6n66_AJo0ynM</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Teipel, Stefan</creator><creator>Grothe, Michel J.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>20160301</creationdate><title>Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?</title><author>Teipel, Stefan ; Grothe, Michel J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c639t-551d363b47ae0fbb50ef29e8a1ba879487f294b604e5354ff2676398a8b9d1a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Aging</topic><topic>Alzheimer Disease - diagnostic imaging</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Atrophy</topic><topic>Cardiology</topic><topic>Cognition</topic><topic>Cognitive Dysfunction - diagnostic imaging</topic><topic>Cognitive Dysfunction - metabolism</topic><topic>Cognitive Dysfunction - physiopathology</topic><topic>Female</topic><topic>Fluorodeoxyglucose F18 - chemistry</topic><topic>Gray Matter - diagnostic imaging</topic><topic>Gray Matter - pathology</topic><topic>Gyrus Cinguli - metabolism</topic><topic>Gyrus Cinguli - physiopathology</topic><topic>Hippocampus - diagnostic imaging</topic><topic>Hippocampus - pathology</topic><topic>Humans</topic><topic>Image Processing, Computer-Assisted</topic><topic>Imaging</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medical diagnosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Nuclear Medicine</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Orthopedics</topic><topic>Pathology</topic><topic>Positron-Emission Tomography</topic><topic>Radiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Teipel, Stefan</creatorcontrib><creatorcontrib>Grothe, Michel J.</creatorcontrib><creatorcontrib>Alzheimer´s Disease Neuroimaging Initiative</creatorcontrib><creatorcontrib>for the Alzheimer´s Disease Neuroimaging Initiative</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European journal of nuclear medicine and molecular imaging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Teipel, Stefan</au><au>Grothe, Michel J.</au><aucorp>Alzheimer´s Disease Neuroimaging Initiative</aucorp><aucorp>for the Alzheimer´s Disease Neuroimaging Initiative</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?</atitle><jtitle>European journal of nuclear medicine and molecular imaging</jtitle><stitle>Eur J Nucl Med Mol Imaging</stitle><addtitle>Eur J Nucl Med Mol Imaging</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>43</volume><issue>3</issue><spage>526</spage><epage>536</epage><pages>526-536</pages><issn>1619-7070</issn><eissn>1619-7089</eissn><abstract>Purpose
Posterior cingulate cortex (PCC) hypometabolism as measured by FDG PET is an indicator of Alzheimer’s disease (AD) in prodromal stages, such as in mild cognitive impairment (MCI), and has been found to be closely associated with hippocampus atrophy in AD dementia. We studied the effects of local and remote atrophy and of local amyloid load on the PCC metabolic signal in patients with different preclinical and clinical stages of AD.
Methods
We determined the volume of the hippocampus and PCC grey matter based on volumetric MRI scans, PCC amyloid load based on AV45 PET, and PCC metabolism based on FDG PET in 667 subjects participating in the Alzheimer’s Disease Neuroimaging Initiative spanning the range from cognitively normal ageing through prodromal AD to AD dementia.
Results
In cognitively normal individuals and those with early MCI, PCC hypometabolism was exclusively associated with hippocampus atrophy, whereas in subjects with late MCI it was associated with both local and remote effects of atrophy as well as local amyloid load. In subjects with AD dementia, PCC hypometabolism was exclusively related to local atrophy.
Conclusion
Our findings suggest that the effects of remote pathology on PCC hypometabolism decrease and the effects of local pathology increase from preclinical to clinical stages of AD, consistent with a progressive disconnection of the PCC from downstream cortical and subcortical brain regions.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26555082</pmid><doi>10.1007/s00259-015-3222-3</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| source | Springer Nature:Jisc Collections:Springer Nature Read and Publish 2023-2025: Springer Reading List |
| subjects | Aged Aging Alzheimer Disease - diagnostic imaging Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Alzheimer's disease Atrophy Cardiology Cognition Cognitive Dysfunction - diagnostic imaging Cognitive Dysfunction - metabolism Cognitive Dysfunction - physiopathology Female Fluorodeoxyglucose F18 - chemistry Gray Matter - diagnostic imaging Gray Matter - pathology Gyrus Cinguli - metabolism Gyrus Cinguli - physiopathology Hippocampus - diagnostic imaging Hippocampus - pathology Humans Image Processing, Computer-Assisted Imaging Magnetic Resonance Imaging Male Medical diagnosis Medicine Medicine & Public Health Metabolism Middle Aged Nuclear Medicine Oncology Original Article Orthopedics Pathology Positron-Emission Tomography Radiology |
| title | Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease? |
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