Alterations of CSF cystatin C levels and their correlations with CSF Αβ40 and Αβ42 levels in patients with Alzheimer's disease, dementia with lewy bodies and the atrophic form of general paresis
Immunohistochemical studies have revealed that cystatin C (CysC) co-localizes with amyloid-β (Αβ) in amyloid-laden vascular walls and in the senile plaque cores of amyloid. In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, i...
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| creator | Zhong, Xiao-Mei Hou, Le Luo, Xin-Ni Shi, Hai-Shan Hu, Guo-Yan He, Hong-Bo Chen, Xin-Ru Zheng, Dong Zhang, Yue-Feng Tan, Yan Liu, Xue-Jun Mu, Nan Chen, Jian-Ping Ning, Yu-Ping |
| description | Immunohistochemical studies have revealed that cystatin C (CysC) co-localizes with amyloid-β (Αβ) in amyloid-laden vascular walls and in the senile plaque cores of amyloid. In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, inhibition of Αβ aggregation, induction of autophagy and induction of cell division. CysC levels may be altered and may have a potential link with cerebrospinal fluid (CSF) Aβ levels in various types of dementia with characteristic amyloid deposits, such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and the atrophic form of general paresis (AF-GP). We assessed the serum and CSF levels of CysC and the CSF levels of Aβ40 and Aβ42 in patients with AD (n = 51), DLB (n = 26) and AF-GP (n = 43) and normal controls (n = 30). Using these samples, we explored the correlation between CSF CysC and CSF Aβ levels. We found that in comparison to the normal control group, both CSF CysC and CSF Aβ42 levels were significantly lower in all three dementia groups (all p |
| doi_str_mv | 10.1371/journal.pone.0055328 |
| format | Article |
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In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, inhibition of Αβ aggregation, induction of autophagy and induction of cell division. CysC levels may be altered and may have a potential link with cerebrospinal fluid (CSF) Aβ levels in various types of dementia with characteristic amyloid deposits, such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and the atrophic form of general paresis (AF-GP). We assessed the serum and CSF levels of CysC and the CSF levels of Aβ40 and Aβ42 in patients with AD (n = 51), DLB (n = 26) and AF-GP (n = 43) and normal controls (n = 30). Using these samples, we explored the correlation between CSF CysC and CSF Aβ levels. We found that in comparison to the normal control group, both CSF CysC and CSF Aβ42 levels were significantly lower in all three dementia groups (all p<0.001); serum CysC levels were the same in the AD and DLB groups, and were lower in the AF-GP group (p = 0.008). The CSF CysC levels were positively correlated with both the CSF Aβ40 and Aβ42 levels in the AD, AF-GP and normal control groups (r = 0.306∼0.657, all p<0.05). Lower CSF CysC levels might be a common feature in dementia with characteristic amyloid deposits. Our results provide evidence for the potential role of CysC involvement in Aβ metabolism and suggest that modulation of the CysC level in the brain might produce a disease-modifying effect in dementia with characteristic amyloid deposits.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0055328</identifier><identifier>PMID: 23383156</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alzheimer Disease - cerebrospinal fluid ; Alzheimer's disease ; Alzheimers disease ; Amyloid ; Amyloid beta-Peptides - cerebrospinal fluid ; Biology ; Biomarkers ; Brain ; Cell division ; Cerebrospinal fluid ; Cognitive ability ; Cores ; Correlation ; Creatine - blood ; Cystatin ; Cystatin C ; Cystatin C - blood ; Cystatin C - cerebrospinal fluid ; Dementia ; Dementia disorders ; Deposits ; Fluid ; Fluids ; Geriatrics ; Glomerular Filtration Rate - physiology ; Hospitals ; Humans ; Immunohistochemistry ; In vivo methods and tests ; Inflammation ; Inhibition ; Lewy bodies ; Lewy Body Disease - cerebrospinal fluid ; Medical laboratories ; Medicine ; Metabolism ; Neurodegeneration ; Neurodegenerative diseases ; Neurology ; Neurosyphilis - cerebrospinal fluid ; Oxidative stress ; Paresis ; Pathology ; Patients ; Peptide Fragments - cerebrospinal fluid ; Phagocytosis ; Rodents ; Senile plaques ; Statistics, Nonparametric</subject><ispartof>PloS one, 2013, Vol.8 (1), p.e55328-e55328</ispartof><rights>2013 Zhong et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Zhong et al 2013 Zhong et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3718-61002a786d6476e987011916751f0c1fc52de384634e0c25caf605277a774ca03</citedby><cites>FETCH-LOGICAL-c3718-61002a786d6476e987011916751f0c1fc52de384634e0c25caf605277a774ca03</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/PMC3558470/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3558470/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2919,4014,23857,27914,27915,27916,53782,53784,79361,79362</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23383156$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Buch, Shilpa J.</contributor><creatorcontrib>Zhong, Xiao-Mei</creatorcontrib><creatorcontrib>Hou, Le</creatorcontrib><creatorcontrib>Luo, Xin-Ni</creatorcontrib><creatorcontrib>Shi, Hai-Shan</creatorcontrib><creatorcontrib>Hu, Guo-Yan</creatorcontrib><creatorcontrib>He, Hong-Bo</creatorcontrib><creatorcontrib>Chen, Xin-Ru</creatorcontrib><creatorcontrib>Zheng, Dong</creatorcontrib><creatorcontrib>Zhang, Yue-Feng</creatorcontrib><creatorcontrib>Tan, Yan</creatorcontrib><creatorcontrib>Liu, Xue-Jun</creatorcontrib><creatorcontrib>Mu, Nan</creatorcontrib><creatorcontrib>Chen, Jian-Ping</creatorcontrib><creatorcontrib>Ning, Yu-Ping</creatorcontrib><title>Alterations of CSF cystatin C levels and their correlations with CSF Αβ40 and Αβ42 levels in patients with Alzheimer's disease, dementia with lewy bodies and the atrophic form of general paresis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Immunohistochemical studies have revealed that cystatin C (CysC) co-localizes with amyloid-β (Αβ) in amyloid-laden vascular walls and in the senile plaque cores of amyloid. In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, inhibition of Αβ aggregation, induction of autophagy and induction of cell division. CysC levels may be altered and may have a potential link with cerebrospinal fluid (CSF) Aβ levels in various types of dementia with characteristic amyloid deposits, such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and the atrophic form of general paresis (AF-GP). We assessed the serum and CSF levels of CysC and the CSF levels of Aβ40 and Aβ42 in patients with AD (n = 51), DLB (n = 26) and AF-GP (n = 43) and normal controls (n = 30). Using these samples, we explored the correlation between CSF CysC and CSF Aβ levels. We found that in comparison to the normal control group, both CSF CysC and CSF Aβ42 levels were significantly lower in all three dementia groups (all p<0.001); serum CysC levels were the same in the AD and DLB groups, and were lower in the AF-GP group (p = 0.008). The CSF CysC levels were positively correlated with both the CSF Aβ40 and Aβ42 levels in the AD, AF-GP and normal control groups (r = 0.306∼0.657, all p<0.05). Lower CSF CysC levels might be a common feature in dementia with characteristic amyloid deposits. Our results provide evidence for the potential role of CysC involvement in Aβ metabolism and suggest that modulation of the CysC level in the brain might produce a disease-modifying effect in dementia with characteristic amyloid deposits.</description><subject>Alzheimer Disease - cerebrospinal fluid</subject><subject>Alzheimer's disease</subject><subject>Alzheimers disease</subject><subject>Amyloid</subject><subject>Amyloid beta-Peptides - cerebrospinal fluid</subject><subject>Biology</subject><subject>Biomarkers</subject><subject>Brain</subject><subject>Cell division</subject><subject>Cerebrospinal fluid</subject><subject>Cognitive ability</subject><subject>Cores</subject><subject>Correlation</subject><subject>Creatine - blood</subject><subject>Cystatin</subject><subject>Cystatin C</subject><subject>Cystatin C - blood</subject><subject>Cystatin C - cerebrospinal fluid</subject><subject>Dementia</subject><subject>Dementia disorders</subject><subject>Deposits</subject><subject>Fluid</subject><subject>Fluids</subject><subject>Geriatrics</subject><subject>Glomerular Filtration Rate - physiology</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In vivo methods and tests</subject><subject>Inflammation</subject><subject>Inhibition</subject><subject>Lewy bodies</subject><subject>Lewy Body Disease - cerebrospinal fluid</subject><subject>Medical laboratories</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neurosyphilis - cerebrospinal fluid</subject><subject>Oxidative stress</subject><subject>Paresis</subject><subject>Pathology</subject><subject>Patients</subject><subject>Peptide Fragments - cerebrospinal fluid</subject><subject>Phagocytosis</subject><subject>Rodents</subject><subject>Senile plaques</subject><subject>Statistics, Nonparametric</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptks1uEzEUhUcIRH_gDRBYYgELEvzvyaZSFFGoVIkFsLYcz53EkWc82JNW4S14lT4Eyz4TTjKJWsRqLPs755575xbFK4LHhCnycRXWsTV-3IUWxhgLwWj5pDglE0ZHkmL29MH5pDhLaZUhVkr5vDihjJWMCHla_Jn6HqLpXWgTCjWafbtEdpP6fNOiGfJwAz4h01aoX4KLyIYYwQ_8reuXO8X97_s7jnfY7kgPwmzSZRjafqCn_lf2aSC-S6hyCUyCD6iCJhPO7BEPtxs0D5WDY2Fk-hi6pbOoDrHZ5lxAm2P77B4hufSieFYbn-Dl8D0vflx--j77Mrr--vlqNr0e2TyyciQJxtSoUlaSKwmTUmFCJkQqQWpsSW0FrYCVXDIO2FJhTS2xoEoZpbg1mJ0Xb_a-nQ9JD78gaZJnjymWRGXiak9Uwax0F11j4kYH4_TuIsSFNrF31oOe1LkYx6KelzWfV7kuJ1IyxSyxpTAke10M1dbzBiqbh5R7fmT6-KV1S70IN5oJUXK1jft-MIjh5xpSrxuXLHhvWgjrnJvmXqkQQmb07T_o_7vje8rGkFKE-hiGYL1dy4NKb9dSD2uZZa8fNnIUHfaQ_QXtLuQm</recordid><startdate>2013</startdate><enddate>2013</enddate><creator>Zhong, Xiao-Mei</creator><creator>Hou, Le</creator><creator>Luo, Xin-Ni</creator><creator>Shi, Hai-Shan</creator><creator>Hu, Guo-Yan</creator><creator>He, Hong-Bo</creator><creator>Chen, Xin-Ru</creator><creator>Zheng, Dong</creator><creator>Zhang, Yue-Feng</creator><creator>Tan, Yan</creator><creator>Liu, Xue-Jun</creator><creator>Mu, Nan</creator><creator>Chen, Jian-Ping</creator><creator>Ning, Yu-Ping</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>2013</creationdate><title>Alterations of CSF cystatin C levels and their correlations with CSF Αβ40 and Αβ42 levels in patients with Alzheimer's disease, dementia with lewy bodies and the atrophic form of general paresis</title><author>Zhong, Xiao-Mei ; Hou, Le ; Luo, Xin-Ni ; Shi, Hai-Shan ; Hu, Guo-Yan ; He, Hong-Bo ; Chen, Xin-Ru ; Zheng, Dong ; Zhang, Yue-Feng ; Tan, Yan ; Liu, Xue-Jun ; Mu, Nan ; Chen, Jian-Ping ; Ning, Yu-Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3718-61002a786d6476e987011916751f0c1fc52de384634e0c25caf605277a774ca03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alzheimer Disease - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhong, Xiao-Mei</au><au>Hou, Le</au><au>Luo, Xin-Ni</au><au>Shi, Hai-Shan</au><au>Hu, Guo-Yan</au><au>He, Hong-Bo</au><au>Chen, Xin-Ru</au><au>Zheng, Dong</au><au>Zhang, Yue-Feng</au><au>Tan, Yan</au><au>Liu, Xue-Jun</au><au>Mu, Nan</au><au>Chen, Jian-Ping</au><au>Ning, Yu-Ping</au><au>Buch, Shilpa J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alterations of CSF cystatin C levels and their correlations with CSF Αβ40 and Αβ42 levels in patients with Alzheimer's disease, dementia with lewy bodies and the atrophic form of general paresis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013</date><risdate>2013</risdate><volume>8</volume><issue>1</issue><spage>e55328</spage><epage>e55328</epage><pages>e55328-e55328</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Immunohistochemical studies have revealed that cystatin C (CysC) co-localizes with amyloid-β (Αβ) in amyloid-laden vascular walls and in the senile plaque cores of amyloid. In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, inhibition of Αβ aggregation, induction of autophagy and induction of cell division. CysC levels may be altered and may have a potential link with cerebrospinal fluid (CSF) Aβ levels in various types of dementia with characteristic amyloid deposits, such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and the atrophic form of general paresis (AF-GP). We assessed the serum and CSF levels of CysC and the CSF levels of Aβ40 and Aβ42 in patients with AD (n = 51), DLB (n = 26) and AF-GP (n = 43) and normal controls (n = 30). Using these samples, we explored the correlation between CSF CysC and CSF Aβ levels. We found that in comparison to the normal control group, both CSF CysC and CSF Aβ42 levels were significantly lower in all three dementia groups (all p<0.001); serum CysC levels were the same in the AD and DLB groups, and were lower in the AF-GP group (p = 0.008). The CSF CysC levels were positively correlated with both the CSF Aβ40 and Aβ42 levels in the AD, AF-GP and normal control groups (r = 0.306∼0.657, all p<0.05). Lower CSF CysC levels might be a common feature in dementia with characteristic amyloid deposits. Our results provide evidence for the potential role of CysC involvement in Aβ metabolism and suggest that modulation of the CysC level in the brain might produce a disease-modifying effect in dementia with characteristic amyloid deposits.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23383156</pmid><doi>10.1371/journal.pone.0055328</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013, Vol.8 (1), p.e55328-e55328 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1328020617 |
| source | MEDLINE; PMC (PubMed Central); Public Library of Science; Full-Text Journals in Chemistry (Open access); Directory of Open Access Journals; EZB Electronic Journals Library |
| subjects | Alzheimer Disease - cerebrospinal fluid Alzheimer's disease Alzheimers disease Amyloid Amyloid beta-Peptides - cerebrospinal fluid Biology Biomarkers Brain Cell division Cerebrospinal fluid Cognitive ability Cores Correlation Creatine - blood Cystatin Cystatin C Cystatin C - blood Cystatin C - cerebrospinal fluid Dementia Dementia disorders Deposits Fluid Fluids Geriatrics Glomerular Filtration Rate - physiology Hospitals Humans Immunohistochemistry In vivo methods and tests Inflammation Inhibition Lewy bodies Lewy Body Disease - cerebrospinal fluid Medical laboratories Medicine Metabolism Neurodegeneration Neurodegenerative diseases Neurology Neurosyphilis - cerebrospinal fluid Oxidative stress Paresis Pathology Patients Peptide Fragments - cerebrospinal fluid Phagocytosis Rodents Senile plaques Statistics, Nonparametric |
| title | Alterations of CSF cystatin C levels and their correlations with CSF Αβ40 and Αβ42 levels in patients with Alzheimer's disease, dementia with lewy bodies and the atrophic form of general paresis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T18%3A37%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Alterations%20of%20CSF%20cystatin%20C%20levels%20and%20their%20correlations%20with%20CSF%20%CE%91%CE%B240%20and%20%CE%91%CE%B242%20levels%20in%20patients%20with%20Alzheimer's%20disease,%20dementia%20with%20lewy%20bodies%20and%20the%20atrophic%20form%20of%20general%20paresis&rft.jtitle=PloS%20one&rft.au=Zhong,%20Xiao-Mei&rft.date=2013&rft.volume=8&rft.issue=1&rft.spage=e55328&rft.epage=e55328&rft.pages=e55328-e55328&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0055328&rft_dat=%3Cproquest_plos_%3E1284625556%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1328020617&rft_id=info:pmid/23383156&rft_doaj_id=oai_doaj_org_article_9fde3405fb8f4bd3844166373c1c85a1&rfr_iscdi=true |