Assessment of Amyloid β Protein in Cerebrospinal Fluid as an Aid in the Diagnosis of Alzheimer's Disease
: The principal constituent of amyloid plaques found in the brains of individuals with Alzheimer's disease (AD) is a 39–42‐amino‐acid protein, amyloid β protein (Aβ). This study examined whether the measurement of Aβ levels in CSF has diagnostic value. There were 108 subjects enrolled in this p...
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Veröffentlicht in: | Journal of neurochemistry 1996-01, Vol.66 (1), p.259-265 |
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description | : The principal constituent of amyloid plaques found in the brains of individuals with Alzheimer's disease (AD) is a 39–42‐amino‐acid protein, amyloid β protein (Aβ). This study examined whether the measurement of Aβ levels in CSF has diagnostic value. There were 108 subjects enrolled in this prospective study: AD (n = 39), non‐AD controls (dementing diseases/syndromes; n = 20), and other (n = 49). CSF was obtained by lumbar puncture, and Aβ concentrations were determined using a dual monoclonal antibody immunoradiometric sandwich assay. The mean Aβ value for the AD group (15.9 ± 6.8 ng/ml) was not significantly different from that for the non‐AD control group (13.0 ± 7.1 ng/ml; p = 0.07), and substantial overlap in results were observed. Aβ values did not correlate with age (r = −0.05, p = 0.59), severity of cognitive impairment (r = 0.22, p = 0.21), or duration of AD symptoms (r = 0.14, p = 0.45). These findings are in conflict with other reports in the literature; discrepant results could be due to the instability of Aβ in CSF. Aβ immunoreactivity decays rapidly under certain conditions, particularly multiple freeze/thaw cycles. Use of a stabilizing sample treatment buffer at the time of lumbar puncture allows storage of CSF without loss of Aβ reactivity. In conclusion, the total CSF Aβ level is not a useful marker for current diagnosis of AD. |
doi_str_mv | 10.1046/j.1471-4159.1996.66010259.x |
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This study examined whether the measurement of Aβ levels in CSF has diagnostic value. There were 108 subjects enrolled in this prospective study: AD (n = 39), non‐AD controls (dementing diseases/syndromes; n = 20), and other (n = 49). CSF was obtained by lumbar puncture, and Aβ concentrations were determined using a dual monoclonal antibody immunoradiometric sandwich assay. The mean Aβ value for the AD group (15.9 ± 6.8 ng/ml) was not significantly different from that for the non‐AD control group (13.0 ± 7.1 ng/ml; p = 0.07), and substantial overlap in results were observed. Aβ values did not correlate with age (r = −0.05, p = 0.59), severity of cognitive impairment (r = 0.22, p = 0.21), or duration of AD symptoms (r = 0.14, p = 0.45). These findings are in conflict with other reports in the literature; discrepant results could be due to the instability of Aβ in CSF. Aβ immunoreactivity decays rapidly under certain conditions, particularly multiple freeze/thaw cycles. Use of a stabilizing sample treatment buffer at the time of lumbar puncture allows storage of CSF without loss of Aβ reactivity. In conclusion, the total CSF Aβ level is not a useful marker for current diagnosis of AD.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1046/j.1471-4159.1996.66010259.x</identifier><identifier>PMID: 8522962</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Alzheimer Disease - cerebrospinal fluid ; Alzheimer Disease - diagnosis ; Alzheimer Disease - epidemiology ; Alzheimer's disease ; Amyloid beta-Peptides - cerebrospinal fluid ; Amyloid β protein ; Autoimmune Diseases - cerebrospinal fluid ; Biological and medical sciences ; Biomarkers ; Cerebrospinal Fluid Proteins - analysis ; CSF ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Diagnosis ; Female ; Humans ; Infection - cerebrospinal fluid ; Inflammation - cerebrospinal fluid ; Male ; Medical sciences ; Mental Disorders - cerebrospinal fluid ; Metabolic Diseases - cerebrospinal fluid ; Middle Aged ; Nervous System Diseases - cerebrospinal fluid ; Neurology ; Predictive Value of Tests ; Prevalence ; Prospective Studies</subject><ispartof>Journal of neurochemistry, 1996-01, Vol.66 (1), p.259-265</ispartof><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4409-7986746388be5fc6c70b6ca41fe4dda46e2d7a006988aef5dc5e17d6ed8c55a23</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1471-4159.1996.66010259.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1471-4159.1996.66010259.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,4010,27900,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2962574$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8522962$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Southwick, Paula C.</creatorcontrib><creatorcontrib>Yamagata, Susan K.</creatorcontrib><creatorcontrib>Echols, Charles L.</creatorcontrib><creatorcontrib>Higson, Gail J.</creatorcontrib><creatorcontrib>Neynaber, Scott A.</creatorcontrib><creatorcontrib>Parson, Robert E.</creatorcontrib><creatorcontrib>Munroe, William A.</creatorcontrib><title>Assessment of Amyloid β Protein in Cerebrospinal Fluid as an Aid in the Diagnosis of Alzheimer's Disease</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>: The principal constituent of amyloid plaques found in the brains of individuals with Alzheimer's disease (AD) is a 39–42‐amino‐acid protein, amyloid β protein (Aβ). This study examined whether the measurement of Aβ levels in CSF has diagnostic value. There were 108 subjects enrolled in this prospective study: AD (n = 39), non‐AD controls (dementing diseases/syndromes; n = 20), and other (n = 49). CSF was obtained by lumbar puncture, and Aβ concentrations were determined using a dual monoclonal antibody immunoradiometric sandwich assay. The mean Aβ value for the AD group (15.9 ± 6.8 ng/ml) was not significantly different from that for the non‐AD control group (13.0 ± 7.1 ng/ml; p = 0.07), and substantial overlap in results were observed. Aβ values did not correlate with age (r = −0.05, p = 0.59), severity of cognitive impairment (r = 0.22, p = 0.21), or duration of AD symptoms (r = 0.14, p = 0.45). These findings are in conflict with other reports in the literature; discrepant results could be due to the instability of Aβ in CSF. Aβ immunoreactivity decays rapidly under certain conditions, particularly multiple freeze/thaw cycles. Use of a stabilizing sample treatment buffer at the time of lumbar puncture allows storage of CSF without loss of Aβ reactivity. In conclusion, the total CSF Aβ level is not a useful marker for current diagnosis of AD.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - cerebrospinal fluid</subject><subject>Alzheimer Disease - diagnosis</subject><subject>Alzheimer Disease - epidemiology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - cerebrospinal fluid</subject><subject>Amyloid β protein</subject><subject>Autoimmune Diseases - cerebrospinal fluid</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>Cerebrospinal Fluid Proteins - analysis</subject><subject>CSF</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Diagnosis</subject><subject>Female</subject><subject>Humans</subject><subject>Infection - cerebrospinal fluid</subject><subject>Inflammation - cerebrospinal fluid</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mental Disorders - cerebrospinal fluid</subject><subject>Metabolic Diseases - cerebrospinal fluid</subject><subject>Middle Aged</subject><subject>Nervous System Diseases - cerebrospinal fluid</subject><subject>Neurology</subject><subject>Predictive Value of Tests</subject><subject>Prevalence</subject><subject>Prospective Studies</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkd1uEzEQha0KVNLSR6hkqYhebWp7vfZaXEWBFlBVuKDXluOdpY68u6knEQ2PxYPwTHhJmluENJJ_zjdj6xxCLjibcibV1XLKpeaF5JWZcmPUVCnGmcinpyMyOWgvyIQxIYqSSfGKnCAuGeNKKn5MjutKCKPEhIQZIiB20K_p0NJZt41DaOjvX_RrGtYQepprDgkWacBV6F2k13GTCYfU9XSWdxlYPwB9H9z3fsCAf-fEnw8QOkiXmAUEh_CavGxdRDjbr6fk_vrDt_nH4vbLzaf57LbwUjJTaFMrLVVZ1wuoWq-8ZgvlneQtyKZxUoFotGNMmbp20FaNr4DrRkFT-6pyojwlb3dzV2l43ACubRfQQ4yuh2GDVmsjZMn4P0GumSiNLjP4bgf67AEmaO0qhc6lreXMjonYpR1dt6PrdkzEPidin3L3-f6ZzaKD5tC7jyDrb_a6Q-9im1zvAx6wkam0zNjNDvsRImz_5wf289081_NF-QcP2ams</recordid><startdate>199601</startdate><enddate>199601</enddate><creator>Southwick, Paula C.</creator><creator>Yamagata, Susan K.</creator><creator>Echols, Charles L.</creator><creator>Higson, Gail J.</creator><creator>Neynaber, Scott A.</creator><creator>Parson, Robert E.</creator><creator>Munroe, William A.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><scope>IQODW</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>199601</creationdate><title>Assessment of Amyloid β Protein in Cerebrospinal Fluid as an Aid in the Diagnosis of Alzheimer's Disease</title><author>Southwick, Paula C. ; Yamagata, Susan K. ; Echols, Charles L. ; Higson, Gail J. ; Neynaber, Scott A. ; Parson, Robert E. ; Munroe, William A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4409-7986746388be5fc6c70b6ca41fe4dda46e2d7a006988aef5dc5e17d6ed8c55a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - cerebrospinal fluid</topic><topic>Alzheimer Disease - diagnosis</topic><topic>Alzheimer Disease - epidemiology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - cerebrospinal fluid</topic><topic>Amyloid β protein</topic><topic>Autoimmune Diseases - cerebrospinal fluid</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>Cerebrospinal Fluid Proteins - analysis</topic><topic>CSF</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Diagnosis</topic><topic>Female</topic><topic>Humans</topic><topic>Infection - cerebrospinal fluid</topic><topic>Inflammation - cerebrospinal fluid</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mental Disorders - cerebrospinal fluid</topic><topic>Metabolic Diseases - cerebrospinal fluid</topic><topic>Middle Aged</topic><topic>Nervous System Diseases - cerebrospinal fluid</topic><topic>Neurology</topic><topic>Predictive Value of Tests</topic><topic>Prevalence</topic><topic>Prospective Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Southwick, Paula C.</creatorcontrib><creatorcontrib>Yamagata, Susan K.</creatorcontrib><creatorcontrib>Echols, Charles L.</creatorcontrib><creatorcontrib>Higson, Gail J.</creatorcontrib><creatorcontrib>Neynaber, Scott A.</creatorcontrib><creatorcontrib>Parson, Robert E.</creatorcontrib><creatorcontrib>Munroe, William A.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Southwick, Paula C.</au><au>Yamagata, Susan K.</au><au>Echols, Charles L.</au><au>Higson, Gail J.</au><au>Neynaber, Scott A.</au><au>Parson, Robert E.</au><au>Munroe, William A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Assessment of Amyloid β Protein in Cerebrospinal Fluid as an Aid in the Diagnosis of Alzheimer's Disease</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>1996-01</date><risdate>1996</risdate><volume>66</volume><issue>1</issue><spage>259</spage><epage>265</epage><pages>259-265</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>: The principal constituent of amyloid plaques found in the brains of individuals with Alzheimer's disease (AD) is a 39–42‐amino‐acid protein, amyloid β protein (Aβ). This study examined whether the measurement of Aβ levels in CSF has diagnostic value. There were 108 subjects enrolled in this prospective study: AD (n = 39), non‐AD controls (dementing diseases/syndromes; n = 20), and other (n = 49). CSF was obtained by lumbar puncture, and Aβ concentrations were determined using a dual monoclonal antibody immunoradiometric sandwich assay. The mean Aβ value for the AD group (15.9 ± 6.8 ng/ml) was not significantly different from that for the non‐AD control group (13.0 ± 7.1 ng/ml; p = 0.07), and substantial overlap in results were observed. Aβ values did not correlate with age (r = −0.05, p = 0.59), severity of cognitive impairment (r = 0.22, p = 0.21), or duration of AD symptoms (r = 0.14, p = 0.45). These findings are in conflict with other reports in the literature; discrepant results could be due to the instability of Aβ in CSF. Aβ immunoreactivity decays rapidly under certain conditions, particularly multiple freeze/thaw cycles. Use of a stabilizing sample treatment buffer at the time of lumbar puncture allows storage of CSF without loss of Aβ reactivity. In conclusion, the total CSF Aβ level is not a useful marker for current diagnosis of AD.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>8522962</pmid><doi>10.1046/j.1471-4159.1996.66010259.x</doi><tpages>7</tpages></addata></record> |
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subjects | Adolescent Adult Aged Aged, 80 and over Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - diagnosis Alzheimer Disease - epidemiology Alzheimer's disease Amyloid beta-Peptides - cerebrospinal fluid Amyloid β protein Autoimmune Diseases - cerebrospinal fluid Biological and medical sciences Biomarkers Cerebrospinal Fluid Proteins - analysis CSF Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Diagnosis Female Humans Infection - cerebrospinal fluid Inflammation - cerebrospinal fluid Male Medical sciences Mental Disorders - cerebrospinal fluid Metabolic Diseases - cerebrospinal fluid Middle Aged Nervous System Diseases - cerebrospinal fluid Neurology Predictive Value of Tests Prevalence Prospective Studies |
title | Assessment of Amyloid β Protein in Cerebrospinal Fluid as an Aid in the Diagnosis of Alzheimer's Disease |
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