Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non‐Alzheimer's disease pathophysiology
Background Suspected non‐Alzheimer's disease pathophysiology (SNAP) is a biomarker concept that encompasses individuals with neuronal injury but without amyloidosis. We aim to investigate the pathophysiology of SNAP, defined as abnormal tau without amyloidosis, in individuals with mild cognitiv...
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| Veröffentlicht in: | Alzheimer's & dementia 2023-03, Vol.19 (3), p.807-820 |
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| creator | Delvenne, Aurore Gobom, Johan Tijms, Betty Bos, Isabelle Reus, Lianne M. Dobricic, Valerija Kate, Mara ten Verhey, Frans Ramakers, Inez Scheltens, Philip Teunissen, Charlotte E. Vandenberghe, Rik Schaeverbeke, Jolien Gabel, Silvy Popp, Julius Peyratout, Gwendoline Martinez‐Lage, Pablo Tainta, Mikel Tsolaki, Magda Freund‐Levi, Yvonne Lovestone, Simon Streffer, Johannes Barkhof, Frederik Bertram, Lars Blennow, Kaj Zetterberg, Henrik Visser, Pieter Jelle Vos, Stephanie J. B. |
| description | Background
Suspected non‐Alzheimer's disease pathophysiology (SNAP) is a biomarker concept that encompasses individuals with neuronal injury but without amyloidosis. We aim to investigate the pathophysiology of SNAP, defined as abnormal tau without amyloidosis, in individuals with mild cognitive impairment (MCI) by cerebrospinal fluid (CSF) proteomics.
Methods
Individuals were classified based on CSF amyloid beta (Aβ)1‐42 (A) and phosphorylated tau (T), as cognitively normal A—T– (CN), MCI A–T+ (MCI‐SNAP), and MCI A+T+ (MCI‐AD). Proteomics analyses, Gene Ontology (GO), brain cell expression, and gene expression analyses in brain regions of interest were performed.
Results
A total of 96 proteins were decreased in MCI‐SNAP compared to CN and MCI‐AD. These proteins were enriched for extracellular matrix (ECM), hemostasis, immune system, protein processing/degradation, lipids, and synapse. Fifty‐one percent were enriched for expression in the choroid plexus.
Conclusion
The pathophysiology of MCI‐SNAP (A–T+) is distinct from that of MCI‐AD. Our findings highlight the need for a different treatment in MCI‐SNAP compared to MCI‐AD. |
| doi_str_mv | 10.1002/alz.12713 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_452777</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2676556062</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4733-55c16067d871018348058618a0d11f9c828e5e34a2855963f7cd29169252e02d3</originalsourceid><addsrcrecordid>eNp9ks2O0zAQxyMEYpeFAy-AfGORyK4_asc5VuVTqsQFOHCx3HiSDjhxiJOtuideAIln5ElwSeltOVgzGv30kzzzz7KnjF4xSvm19bdXjBdM3MvOmZQ8l7wo7596Rc-yRzF-pXRBNZMPszMhVam15ufZzxUMsBlC7LGzntR-Qkf6IYwQWqwOXY0eu4aEmmDn8AbdZH0kOxy3pEXvSBWaDke8AYJtb3FooRuJ7RyJU-yhGsGRLnS_f_xa-tstYAvD80gcRrARSG_Hbei3-4jBh2b_OHtQJzs8OdaL7NOb1x9X7_L1h7fvV8t1Xi0KIXIpK6aoKpwuGGVaLDSVWjFtqWOsLivNNUgQC8u1lKUSdVE5XjJVcsmBcicusnz2xh3008b0A7Z22Jtg0RxH31IHZpE2WRT_5ZupN2nUTAdecEpVmfiXd_Kv8PPShKFJbzJlqbhI-OWMp3V_nyCOpsVYgfe2gzBFw1WhpEw_5gl9MaNVulkcoD65GTWHMJgUBvM3DIl9dtROmxbcifx3_QRcz8AOPezvNpnl-sus_AOpaMLW</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2676556062</pqid></control><display><type>article</type><title>Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non‐Alzheimer's disease pathophysiology</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>SWEPUB Freely available online</source><creator>Delvenne, Aurore ; Gobom, Johan ; Tijms, Betty ; Bos, Isabelle ; Reus, Lianne M. ; Dobricic, Valerija ; Kate, Mara ten ; Verhey, Frans ; Ramakers, Inez ; Scheltens, Philip ; Teunissen, Charlotte E. ; Vandenberghe, Rik ; Schaeverbeke, Jolien ; Gabel, Silvy ; Popp, Julius ; Peyratout, Gwendoline ; Martinez‐Lage, Pablo ; Tainta, Mikel ; Tsolaki, Magda ; Freund‐Levi, Yvonne ; Lovestone, Simon ; Streffer, Johannes ; Barkhof, Frederik ; Bertram, Lars ; Blennow, Kaj ; Zetterberg, Henrik ; Visser, Pieter Jelle ; Vos, Stephanie J. B.</creator><creatorcontrib>Delvenne, Aurore ; Gobom, Johan ; Tijms, Betty ; Bos, Isabelle ; Reus, Lianne M. ; Dobricic, Valerija ; Kate, Mara ten ; Verhey, Frans ; Ramakers, Inez ; Scheltens, Philip ; Teunissen, Charlotte E. ; Vandenberghe, Rik ; Schaeverbeke, Jolien ; Gabel, Silvy ; Popp, Julius ; Peyratout, Gwendoline ; Martinez‐Lage, Pablo ; Tainta, Mikel ; Tsolaki, Magda ; Freund‐Levi, Yvonne ; Lovestone, Simon ; Streffer, Johannes ; Barkhof, Frederik ; Bertram, Lars ; Blennow, Kaj ; Zetterberg, Henrik ; Visser, Pieter Jelle ; Vos, Stephanie J. B.</creatorcontrib><description>Background
Suspected non‐Alzheimer's disease pathophysiology (SNAP) is a biomarker concept that encompasses individuals with neuronal injury but without amyloidosis. We aim to investigate the pathophysiology of SNAP, defined as abnormal tau without amyloidosis, in individuals with mild cognitive impairment (MCI) by cerebrospinal fluid (CSF) proteomics.
Methods
Individuals were classified based on CSF amyloid beta (Aβ)1‐42 (A) and phosphorylated tau (T), as cognitively normal A—T– (CN), MCI A–T+ (MCI‐SNAP), and MCI A+T+ (MCI‐AD). Proteomics analyses, Gene Ontology (GO), brain cell expression, and gene expression analyses in brain regions of interest were performed.
Results
A total of 96 proteins were decreased in MCI‐SNAP compared to CN and MCI‐AD. These proteins were enriched for extracellular matrix (ECM), hemostasis, immune system, protein processing/degradation, lipids, and synapse. Fifty‐one percent were enriched for expression in the choroid plexus.
Conclusion
The pathophysiology of MCI‐SNAP (A–T+) is distinct from that of MCI‐AD. Our findings highlight the need for a different treatment in MCI‐SNAP compared to MCI‐AD.</description><identifier>ISSN: 1552-5260</identifier><identifier>ISSN: 1552-5279</identifier><identifier>EISSN: 1552-5279</identifier><identifier>DOI: 10.1002/alz.12713</identifier><identifier>PMID: 35698882</identifier><language>eng</language><publisher>United States</publisher><subject>adult ; Aged ; Alzheimer Disease - cerebrospinal fluid ; Alzheimer's disease ; Amyloid beta-Peptides - cerebrospinal fluid ; biomarkers ; Biomarkers - cerebrospinal fluid ; cerebrospinal fluid ; Cognitive Dysfunction - cerebrospinal fluid ; disease pathophysiology ; Female ; Humans ; impairment ; Male ; Middle Aged ; mild cognitive ; mild cognitive impairment ; Neurologi ; Neurology ; Neurosciences & Neurology ; pathophysiology ; Peptide Fragments - cerebrospinal fluid ; protein ; Proteomics ; suspected non-Alzheimer's ; suspected non-Alzheimer's disease pathophysiology ; tau ; tau Proteins - cerebrospinal fluid</subject><ispartof>Alzheimer's & dementia, 2023-03, Vol.19 (3), p.807-820</ispartof><rights>2022 The Authors. published by Wiley Periodicals LLC on behalf of Alzheimer's Association.</rights><rights>2022 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4733-55c16067d871018348058618a0d11f9c828e5e34a2855963f7cd29169252e02d3</citedby><cites>FETCH-LOGICAL-c4733-55c16067d871018348058618a0d11f9c828e5e34a2855963f7cd29169252e02d3</cites><orcidid>0000-0001-8724-3010</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Falz.12713$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Falz.12713$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,776,780,881,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35698882$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-99623$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/320069$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:149845816$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Delvenne, Aurore</creatorcontrib><creatorcontrib>Gobom, Johan</creatorcontrib><creatorcontrib>Tijms, Betty</creatorcontrib><creatorcontrib>Bos, Isabelle</creatorcontrib><creatorcontrib>Reus, Lianne M.</creatorcontrib><creatorcontrib>Dobricic, Valerija</creatorcontrib><creatorcontrib>Kate, Mara ten</creatorcontrib><creatorcontrib>Verhey, Frans</creatorcontrib><creatorcontrib>Ramakers, Inez</creatorcontrib><creatorcontrib>Scheltens, Philip</creatorcontrib><creatorcontrib>Teunissen, Charlotte E.</creatorcontrib><creatorcontrib>Vandenberghe, Rik</creatorcontrib><creatorcontrib>Schaeverbeke, Jolien</creatorcontrib><creatorcontrib>Gabel, Silvy</creatorcontrib><creatorcontrib>Popp, Julius</creatorcontrib><creatorcontrib>Peyratout, Gwendoline</creatorcontrib><creatorcontrib>Martinez‐Lage, Pablo</creatorcontrib><creatorcontrib>Tainta, Mikel</creatorcontrib><creatorcontrib>Tsolaki, Magda</creatorcontrib><creatorcontrib>Freund‐Levi, Yvonne</creatorcontrib><creatorcontrib>Lovestone, Simon</creatorcontrib><creatorcontrib>Streffer, Johannes</creatorcontrib><creatorcontrib>Barkhof, Frederik</creatorcontrib><creatorcontrib>Bertram, Lars</creatorcontrib><creatorcontrib>Blennow, Kaj</creatorcontrib><creatorcontrib>Zetterberg, Henrik</creatorcontrib><creatorcontrib>Visser, Pieter Jelle</creatorcontrib><creatorcontrib>Vos, Stephanie J. B.</creatorcontrib><title>Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non‐Alzheimer's disease pathophysiology</title><title>Alzheimer's & dementia</title><addtitle>Alzheimers Dement</addtitle><description>Background
Suspected non‐Alzheimer's disease pathophysiology (SNAP) is a biomarker concept that encompasses individuals with neuronal injury but without amyloidosis. We aim to investigate the pathophysiology of SNAP, defined as abnormal tau without amyloidosis, in individuals with mild cognitive impairment (MCI) by cerebrospinal fluid (CSF) proteomics.
Methods
Individuals were classified based on CSF amyloid beta (Aβ)1‐42 (A) and phosphorylated tau (T), as cognitively normal A—T– (CN), MCI A–T+ (MCI‐SNAP), and MCI A+T+ (MCI‐AD). Proteomics analyses, Gene Ontology (GO), brain cell expression, and gene expression analyses in brain regions of interest were performed.
Results
A total of 96 proteins were decreased in MCI‐SNAP compared to CN and MCI‐AD. These proteins were enriched for extracellular matrix (ECM), hemostasis, immune system, protein processing/degradation, lipids, and synapse. Fifty‐one percent were enriched for expression in the choroid plexus.
Conclusion
The pathophysiology of MCI‐SNAP (A–T+) is distinct from that of MCI‐AD. Our findings highlight the need for a different treatment in MCI‐SNAP compared to MCI‐AD.</description><subject>adult</subject><subject>Aged</subject><subject>Alzheimer Disease - cerebrospinal fluid</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - cerebrospinal fluid</subject><subject>biomarkers</subject><subject>Biomarkers - cerebrospinal fluid</subject><subject>cerebrospinal fluid</subject><subject>Cognitive Dysfunction - cerebrospinal fluid</subject><subject>disease pathophysiology</subject><subject>Female</subject><subject>Humans</subject><subject>impairment</subject><subject>Male</subject><subject>Middle Aged</subject><subject>mild cognitive</subject><subject>mild cognitive impairment</subject><subject>Neurologi</subject><subject>Neurology</subject><subject>Neurosciences & Neurology</subject><subject>pathophysiology</subject><subject>Peptide Fragments - cerebrospinal fluid</subject><subject>protein</subject><subject>Proteomics</subject><subject>suspected non-Alzheimer's</subject><subject>suspected non-Alzheimer's disease pathophysiology</subject><subject>tau</subject><subject>tau Proteins - cerebrospinal fluid</subject><issn>1552-5260</issn><issn>1552-5279</issn><issn>1552-5279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNp9ks2O0zAQxyMEYpeFAy-AfGORyK4_asc5VuVTqsQFOHCx3HiSDjhxiJOtuideAIln5ElwSeltOVgzGv30kzzzz7KnjF4xSvm19bdXjBdM3MvOmZQ8l7wo7596Rc-yRzF-pXRBNZMPszMhVam15ufZzxUMsBlC7LGzntR-Qkf6IYwQWqwOXY0eu4aEmmDn8AbdZH0kOxy3pEXvSBWaDke8AYJtb3FooRuJ7RyJU-yhGsGRLnS_f_xa-tstYAvD80gcRrARSG_Hbei3-4jBh2b_OHtQJzs8OdaL7NOb1x9X7_L1h7fvV8t1Xi0KIXIpK6aoKpwuGGVaLDSVWjFtqWOsLivNNUgQC8u1lKUSdVE5XjJVcsmBcicusnz2xh3008b0A7Z22Jtg0RxH31IHZpE2WRT_5ZupN2nUTAdecEpVmfiXd_Kv8PPShKFJbzJlqbhI-OWMp3V_nyCOpsVYgfe2gzBFw1WhpEw_5gl9MaNVulkcoD65GTWHMJgUBvM3DIl9dtROmxbcifx3_QRcz8AOPezvNpnl-sus_AOpaMLW</recordid><startdate>202303</startdate><enddate>202303</enddate><creator>Delvenne, Aurore</creator><creator>Gobom, Johan</creator><creator>Tijms, Betty</creator><creator>Bos, Isabelle</creator><creator>Reus, Lianne M.</creator><creator>Dobricic, Valerija</creator><creator>Kate, Mara ten</creator><creator>Verhey, Frans</creator><creator>Ramakers, Inez</creator><creator>Scheltens, Philip</creator><creator>Teunissen, Charlotte E.</creator><creator>Vandenberghe, Rik</creator><creator>Schaeverbeke, Jolien</creator><creator>Gabel, Silvy</creator><creator>Popp, Julius</creator><creator>Peyratout, Gwendoline</creator><creator>Martinez‐Lage, Pablo</creator><creator>Tainta, Mikel</creator><creator>Tsolaki, Magda</creator><creator>Freund‐Levi, Yvonne</creator><creator>Lovestone, Simon</creator><creator>Streffer, Johannes</creator><creator>Barkhof, Frederik</creator><creator>Bertram, Lars</creator><creator>Blennow, Kaj</creator><creator>Zetterberg, Henrik</creator><creator>Visser, Pieter Jelle</creator><creator>Vos, Stephanie J. B.</creator><scope>24P</scope><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>7X8</scope><scope>AABEP</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>D91</scope><scope>ZZAVC</scope><scope>F1U</scope><orcidid>https://orcid.org/0000-0001-8724-3010</orcidid></search><sort><creationdate>202303</creationdate><title>Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non‐Alzheimer's disease pathophysiology</title><author>Delvenne, Aurore ; Gobom, Johan ; Tijms, Betty ; Bos, Isabelle ; Reus, Lianne M. ; Dobricic, Valerija ; Kate, Mara ten ; Verhey, Frans ; Ramakers, Inez ; Scheltens, Philip ; Teunissen, Charlotte E. ; Vandenberghe, Rik ; Schaeverbeke, Jolien ; Gabel, Silvy ; Popp, Julius ; Peyratout, Gwendoline ; Martinez‐Lage, Pablo ; Tainta, Mikel ; Tsolaki, Magda ; Freund‐Levi, Yvonne ; Lovestone, Simon ; Streffer, Johannes ; Barkhof, Frederik ; Bertram, Lars ; Blennow, Kaj ; Zetterberg, Henrik ; Visser, Pieter Jelle ; Vos, Stephanie J. B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4733-55c16067d871018348058618a0d11f9c828e5e34a2855963f7cd29169252e02d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>adult</topic><topic>Aged</topic><topic>Alzheimer Disease - cerebrospinal fluid</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - cerebrospinal fluid</topic><topic>biomarkers</topic><topic>Biomarkers - cerebrospinal fluid</topic><topic>cerebrospinal fluid</topic><topic>Cognitive Dysfunction - cerebrospinal fluid</topic><topic>disease pathophysiology</topic><topic>Female</topic><topic>Humans</topic><topic>impairment</topic><topic>Male</topic><topic>Middle Aged</topic><topic>mild cognitive</topic><topic>mild cognitive impairment</topic><topic>Neurologi</topic><topic>Neurology</topic><topic>Neurosciences & Neurology</topic><topic>pathophysiology</topic><topic>Peptide Fragments - cerebrospinal fluid</topic><topic>protein</topic><topic>Proteomics</topic><topic>suspected non-Alzheimer's</topic><topic>suspected non-Alzheimer's disease pathophysiology</topic><topic>tau</topic><topic>tau Proteins - cerebrospinal fluid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Delvenne, Aurore</creatorcontrib><creatorcontrib>Gobom, Johan</creatorcontrib><creatorcontrib>Tijms, Betty</creatorcontrib><creatorcontrib>Bos, Isabelle</creatorcontrib><creatorcontrib>Reus, Lianne M.</creatorcontrib><creatorcontrib>Dobricic, Valerija</creatorcontrib><creatorcontrib>Kate, Mara ten</creatorcontrib><creatorcontrib>Verhey, Frans</creatorcontrib><creatorcontrib>Ramakers, Inez</creatorcontrib><creatorcontrib>Scheltens, Philip</creatorcontrib><creatorcontrib>Teunissen, Charlotte E.</creatorcontrib><creatorcontrib>Vandenberghe, Rik</creatorcontrib><creatorcontrib>Schaeverbeke, Jolien</creatorcontrib><creatorcontrib>Gabel, Silvy</creatorcontrib><creatorcontrib>Popp, Julius</creatorcontrib><creatorcontrib>Peyratout, Gwendoline</creatorcontrib><creatorcontrib>Martinez‐Lage, Pablo</creatorcontrib><creatorcontrib>Tainta, Mikel</creatorcontrib><creatorcontrib>Tsolaki, Magda</creatorcontrib><creatorcontrib>Freund‐Levi, Yvonne</creatorcontrib><creatorcontrib>Lovestone, Simon</creatorcontrib><creatorcontrib>Streffer, Johannes</creatorcontrib><creatorcontrib>Barkhof, Frederik</creatorcontrib><creatorcontrib>Bertram, Lars</creatorcontrib><creatorcontrib>Blennow, Kaj</creatorcontrib><creatorcontrib>Zetterberg, Henrik</creatorcontrib><creatorcontrib>Visser, Pieter Jelle</creatorcontrib><creatorcontrib>Vos, Stephanie J. B.</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SWEPUB Örebro universitet full text</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Örebro universitet</collection><collection>SwePub Articles full text</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Alzheimer's & dementia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Delvenne, Aurore</au><au>Gobom, Johan</au><au>Tijms, Betty</au><au>Bos, Isabelle</au><au>Reus, Lianne M.</au><au>Dobricic, Valerija</au><au>Kate, Mara ten</au><au>Verhey, Frans</au><au>Ramakers, Inez</au><au>Scheltens, Philip</au><au>Teunissen, Charlotte E.</au><au>Vandenberghe, Rik</au><au>Schaeverbeke, Jolien</au><au>Gabel, Silvy</au><au>Popp, Julius</au><au>Peyratout, Gwendoline</au><au>Martinez‐Lage, Pablo</au><au>Tainta, Mikel</au><au>Tsolaki, Magda</au><au>Freund‐Levi, Yvonne</au><au>Lovestone, Simon</au><au>Streffer, Johannes</au><au>Barkhof, Frederik</au><au>Bertram, Lars</au><au>Blennow, Kaj</au><au>Zetterberg, Henrik</au><au>Visser, Pieter Jelle</au><au>Vos, Stephanie J. B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non‐Alzheimer's disease pathophysiology</atitle><jtitle>Alzheimer's & dementia</jtitle><addtitle>Alzheimers Dement</addtitle><date>2023-03</date><risdate>2023</risdate><volume>19</volume><issue>3</issue><spage>807</spage><epage>820</epage><pages>807-820</pages><issn>1552-5260</issn><issn>1552-5279</issn><eissn>1552-5279</eissn><abstract>Background
Suspected non‐Alzheimer's disease pathophysiology (SNAP) is a biomarker concept that encompasses individuals with neuronal injury but without amyloidosis. We aim to investigate the pathophysiology of SNAP, defined as abnormal tau without amyloidosis, in individuals with mild cognitive impairment (MCI) by cerebrospinal fluid (CSF) proteomics.
Methods
Individuals were classified based on CSF amyloid beta (Aβ)1‐42 (A) and phosphorylated tau (T), as cognitively normal A—T– (CN), MCI A–T+ (MCI‐SNAP), and MCI A+T+ (MCI‐AD). Proteomics analyses, Gene Ontology (GO), brain cell expression, and gene expression analyses in brain regions of interest were performed.
Results
A total of 96 proteins were decreased in MCI‐SNAP compared to CN and MCI‐AD. These proteins were enriched for extracellular matrix (ECM), hemostasis, immune system, protein processing/degradation, lipids, and synapse. Fifty‐one percent were enriched for expression in the choroid plexus.
Conclusion
The pathophysiology of MCI‐SNAP (A–T+) is distinct from that of MCI‐AD. Our findings highlight the need for a different treatment in MCI‐SNAP compared to MCI‐AD.</abstract><cop>United States</cop><pmid>35698882</pmid><doi>10.1002/alz.12713</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-8724-3010</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Alzheimer's & dementia, 2023-03, Vol.19 (3), p.807-820 |
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| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; SWEPUB Freely available online |
| subjects | adult Aged Alzheimer Disease - cerebrospinal fluid Alzheimer's disease Amyloid beta-Peptides - cerebrospinal fluid biomarkers Biomarkers - cerebrospinal fluid cerebrospinal fluid Cognitive Dysfunction - cerebrospinal fluid disease pathophysiology Female Humans impairment Male Middle Aged mild cognitive mild cognitive impairment Neurologi Neurology Neurosciences & Neurology pathophysiology Peptide Fragments - cerebrospinal fluid protein Proteomics suspected non-Alzheimer's suspected non-Alzheimer's disease pathophysiology tau tau Proteins - cerebrospinal fluid |
| title | Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non‐Alzheimer's disease pathophysiology |
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