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Associations of cerebrospinal fluid complement proteins with Alzheimer's pathology, cognition, and brain structure in non-dementia elderly
Cerebrospinal fluid (CSF) complement activation is a key part of neuroinflammation that occurs in the early stages of Alzheimer's disease (AD). However, the associations of CSF complement proteins with AD pathology, cognition, and structural neuroimaging biomarkers for AD have been rarely inves...
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Published in: | Alzheimer's research & therapy 2024-01, Vol.16 (1), p.12-12, Article 12 |
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description | Cerebrospinal fluid (CSF) complement activation is a key part of neuroinflammation that occurs in the early stages of Alzheimer's disease (AD). However, the associations of CSF complement proteins with AD pathology, cognition, and structural neuroimaging biomarkers for AD have been rarely investigated.
A total of 210 participants (125 mild cognitive impairment [MCI] patients and 85 normal controls) were included from Alzheimer's Disease Neuroimaging Initiative (ADNI) database who measured AD pathology, cognition, and neuroimaging at baseline and every 12 months. The mixed-effect linear models were utilized to investigate longitudinal associations of CSF complement proteins with AD pathology, cognition, and neuroimaging in cognitively normal (CN) and mild cognitive impairment (MCI) subjects. Causal mediation analyses were conducted to explore the potential mediators between CSF complement proteins and cognitive changes.
We found that the subjects with low CSF complement protein levels at baseline had worse outcomes in AD pathology, indicated by their lowest concentrations observed in A + and A + T + individuals. The reduced CSF complement proteins were associated with faster accumulation of tau among CN subjects and with cognitive decline and greater brain atrophy of specific regions among MCI subjects. Furthermore, mediation analyses showed that the effects of CSF complement proteins on cognitive performance were partially mediated by regional brain structures (mediation proportions range from 19.78 to 94.92%; p |
doi_str_mv | 10.1186/s13195-023-01377-5 |
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A total of 210 participants (125 mild cognitive impairment [MCI] patients and 85 normal controls) were included from Alzheimer's Disease Neuroimaging Initiative (ADNI) database who measured AD pathology, cognition, and neuroimaging at baseline and every 12 months. The mixed-effect linear models were utilized to investigate longitudinal associations of CSF complement proteins with AD pathology, cognition, and neuroimaging in cognitively normal (CN) and mild cognitive impairment (MCI) subjects. Causal mediation analyses were conducted to explore the potential mediators between CSF complement proteins and cognitive changes.
We found that the subjects with low CSF complement protein levels at baseline had worse outcomes in AD pathology, indicated by their lowest concentrations observed in A + and A + T + individuals. The reduced CSF complement proteins were associated with faster accumulation of tau among CN subjects and with cognitive decline and greater brain atrophy of specific regions among MCI subjects. Furthermore, mediation analyses showed that the effects of CSF complement proteins on cognitive performance were partially mediated by regional brain structures (mediation proportions range from 19.78 to 94.92%; p < 0.05).
This study demonstrated that CSF complement proteins were involved in the early progression of AD. Our results indicated that regional brain atrophy might be a plausible way to connect CSF complement protein levels and cognition.</description><identifier>ISSN: 1758-9193</identifier><identifier>EISSN: 1758-9193</identifier><identifier>DOI: 10.1186/s13195-023-01377-5</identifier><identifier>PMID: 38238858</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Advertising executives ; Aged ; Alzheimer's disease ; Biomarkers ; Brain ; Brain structure ; Cerebrospinal fluid proteins ; Cognition ; Cognition & reasoning ; Cognition disorders ; Complement ; Complement (Immunology) ; Dementia ; Development and progression ; Health aspects ; Magnetic resonance imaging ; Measurement ; Mediation ; Pathology ; Risk factors ; Size</subject><ispartof>Alzheimer's research & therapy, 2024-01, Vol.16 (1), p.12-12, Article 12</ispartof><rights>2024. The Author(s).</rights><rights>COPYRIGHT 2024 BioMed Central Ltd.</rights><rights>2024. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c595t-3dcaabaf06922b320b44f3c4dbfc562dd16e98d607caa7a3a3e1501117db7b0c3</citedby><cites>FETCH-LOGICAL-c595t-3dcaabaf06922b320b44f3c4dbfc562dd16e98d607caa7a3a3e1501117db7b0c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10795368/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2925658476?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25752,27923,27924,37011,37012,44589,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38238858$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Meng</creatorcontrib><creatorcontrib>Ma, Ya-Hui</creatorcontrib><creatorcontrib>Guo, Yun</creatorcontrib><creatorcontrib>Liu, Jia-Yao</creatorcontrib><creatorcontrib>Tan, Lan</creatorcontrib><creatorcontrib>Alzheimer’s Disease Neuroimaging Initiative</creatorcontrib><creatorcontrib>on behalf of Alzheimer’s Disease Neuroimaging Initiative</creatorcontrib><title>Associations of cerebrospinal fluid complement proteins with Alzheimer's pathology, cognition, and brain structure in non-dementia elderly</title><title>Alzheimer's research & therapy</title><addtitle>Alzheimers Res Ther</addtitle><description>Cerebrospinal fluid (CSF) complement activation is a key part of neuroinflammation that occurs in the early stages of Alzheimer's disease (AD). However, the associations of CSF complement proteins with AD pathology, cognition, and structural neuroimaging biomarkers for AD have been rarely investigated.
A total of 210 participants (125 mild cognitive impairment [MCI] patients and 85 normal controls) were included from Alzheimer's Disease Neuroimaging Initiative (ADNI) database who measured AD pathology, cognition, and neuroimaging at baseline and every 12 months. The mixed-effect linear models were utilized to investigate longitudinal associations of CSF complement proteins with AD pathology, cognition, and neuroimaging in cognitively normal (CN) and mild cognitive impairment (MCI) subjects. Causal mediation analyses were conducted to explore the potential mediators between CSF complement proteins and cognitive changes.
We found that the subjects with low CSF complement protein levels at baseline had worse outcomes in AD pathology, indicated by their lowest concentrations observed in A + and A + T + individuals. The reduced CSF complement proteins were associated with faster accumulation of tau among CN subjects and with cognitive decline and greater brain atrophy of specific regions among MCI subjects. Furthermore, mediation analyses showed that the effects of CSF complement proteins on cognitive performance were partially mediated by regional brain structures (mediation proportions range from 19.78 to 94.92%; p < 0.05).
This study demonstrated that CSF complement proteins were involved in the early progression of AD. Our results indicated that regional brain atrophy might be a plausible way to connect CSF complement protein levels and cognition.</description><subject>Advertising executives</subject><subject>Aged</subject><subject>Alzheimer's disease</subject><subject>Biomarkers</subject><subject>Brain</subject><subject>Brain structure</subject><subject>Cerebrospinal fluid proteins</subject><subject>Cognition</subject><subject>Cognition & reasoning</subject><subject>Cognition disorders</subject><subject>Complement</subject><subject>Complement (Immunology)</subject><subject>Dementia</subject><subject>Development and progression</subject><subject>Health aspects</subject><subject>Magnetic resonance imaging</subject><subject>Measurement</subject><subject>Mediation</subject><subject>Pathology</subject><subject>Risk factors</subject><subject>Size</subject><issn>1758-9193</issn><issn>1758-9193</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkt2O1CAYhhujcdfVG_DAkJioB9uVn1LokZls_NlkE0_0mFCgUyYUKlDNeAletczMus4YwwEUnu9p4Hur6jmCVwjx9m1CBHW0hpjUEBHGavqgOkeM8rpDHXl4tD6rnqS0gbBtMW8eV2eEY8I55efVr1VKQVmZbfAJhAEoE00fQ5qtlw4MbrEaqDDNzkzGZzDHkI0t6A-bR7ByP0djJxNfJzDLPAYX1tvLwq-93RkvgfQa9FFaD1KOi8pLNKB8-OBrvTdaCYzTJrrt0-rRIF0yz-7mi-rrh_dfrj_Vt58_3lyvbmtFO5propWUvRxg22HcEwz7phmIanQ_KNpirVFrOq5byArHJJHEIAoRQkz3rIeKXFQ3B68OciPmaCcZtyJIK_YbIa6FjNkqZwSWHYWkk4QT1gys7enQG40QZhpqqkxxvTu45qWfjFblQlG6E-npibejWIfvAkHWUdLyYnhzZ4jh22JSFpNNyjgnvQlLErgrXaSlu11BX_6DbsISS5t2FKYt5Q1r_1JrWW5g_RDKj9VOKlaM45IY3sBCXf2HKqN0xargzWDL_knBq6OC0UiXxxTcsg_OKYgPoCopStEM96-BoNjlVhxyK0puxT63gpaiF8fveF_yJ6jkNw_Q6oI</recordid><startdate>20240118</startdate><enddate>20240118</enddate><creator>Li, Meng</creator><creator>Ma, Ya-Hui</creator><creator>Guo, Yun</creator><creator>Liu, Jia-Yao</creator><creator>Tan, Lan</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20240118</creationdate><title>Associations of cerebrospinal fluid complement proteins with Alzheimer's pathology, cognition, and brain structure in non-dementia elderly</title><author>Li, Meng ; Ma, Ya-Hui ; Guo, Yun ; Liu, Jia-Yao ; Tan, Lan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c595t-3dcaabaf06922b320b44f3c4dbfc562dd16e98d607caa7a3a3e1501117db7b0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Advertising executives</topic><topic>Aged</topic><topic>Alzheimer's disease</topic><topic>Biomarkers</topic><topic>Brain</topic><topic>Brain structure</topic><topic>Cerebrospinal fluid proteins</topic><topic>Cognition</topic><topic>Cognition & reasoning</topic><topic>Cognition disorders</topic><topic>Complement</topic><topic>Complement (Immunology)</topic><topic>Dementia</topic><topic>Development and progression</topic><topic>Health aspects</topic><topic>Magnetic resonance imaging</topic><topic>Measurement</topic><topic>Mediation</topic><topic>Pathology</topic><topic>Risk factors</topic><topic>Size</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Meng</creatorcontrib><creatorcontrib>Ma, Ya-Hui</creatorcontrib><creatorcontrib>Guo, Yun</creatorcontrib><creatorcontrib>Liu, Jia-Yao</creatorcontrib><creatorcontrib>Tan, Lan</creatorcontrib><creatorcontrib>Alzheimer’s Disease Neuroimaging Initiative</creatorcontrib><creatorcontrib>on behalf of Alzheimer’s Disease Neuroimaging Initiative</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Alzheimer's research & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Meng</au><au>Ma, Ya-Hui</au><au>Guo, Yun</au><au>Liu, Jia-Yao</au><au>Tan, Lan</au><aucorp>Alzheimer’s Disease Neuroimaging Initiative</aucorp><aucorp>on behalf of Alzheimer’s Disease Neuroimaging Initiative</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Associations of cerebrospinal fluid complement proteins with Alzheimer's pathology, cognition, and brain structure in non-dementia elderly</atitle><jtitle>Alzheimer's research & therapy</jtitle><addtitle>Alzheimers Res Ther</addtitle><date>2024-01-18</date><risdate>2024</risdate><volume>16</volume><issue>1</issue><spage>12</spage><epage>12</epage><pages>12-12</pages><artnum>12</artnum><issn>1758-9193</issn><eissn>1758-9193</eissn><abstract>Cerebrospinal fluid (CSF) complement activation is a key part of neuroinflammation that occurs in the early stages of Alzheimer's disease (AD). However, the associations of CSF complement proteins with AD pathology, cognition, and structural neuroimaging biomarkers for AD have been rarely investigated.
A total of 210 participants (125 mild cognitive impairment [MCI] patients and 85 normal controls) were included from Alzheimer's Disease Neuroimaging Initiative (ADNI) database who measured AD pathology, cognition, and neuroimaging at baseline and every 12 months. The mixed-effect linear models were utilized to investigate longitudinal associations of CSF complement proteins with AD pathology, cognition, and neuroimaging in cognitively normal (CN) and mild cognitive impairment (MCI) subjects. Causal mediation analyses were conducted to explore the potential mediators between CSF complement proteins and cognitive changes.
We found that the subjects with low CSF complement protein levels at baseline had worse outcomes in AD pathology, indicated by their lowest concentrations observed in A + and A + T + individuals. The reduced CSF complement proteins were associated with faster accumulation of tau among CN subjects and with cognitive decline and greater brain atrophy of specific regions among MCI subjects. Furthermore, mediation analyses showed that the effects of CSF complement proteins on cognitive performance were partially mediated by regional brain structures (mediation proportions range from 19.78 to 94.92%; p < 0.05).
This study demonstrated that CSF complement proteins were involved in the early progression of AD. Our results indicated that regional brain atrophy might be a plausible way to connect CSF complement protein levels and cognition.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>38238858</pmid><doi>10.1186/s13195-023-01377-5</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Advertising executives Aged Alzheimer's disease Biomarkers Brain Brain structure Cerebrospinal fluid proteins Cognition Cognition & reasoning Cognition disorders Complement Complement (Immunology) Dementia Development and progression Health aspects Magnetic resonance imaging Measurement Mediation Pathology Risk factors Size |
title | Associations of cerebrospinal fluid complement proteins with Alzheimer's pathology, cognition, and brain structure in non-dementia elderly |
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