Biological confounders for the values of cerebrospinal fluid proteins in Parkinson's disease and related disorders.
Identifieur interne : 000142 ( PubMed/Curation ); précédent : 000141; suivant : 000143Biological confounders for the values of cerebrospinal fluid proteins in Parkinson's disease and related disorders.
Auteurs : Brit Mollenhauer [Allemagne] ; Lucilla Parnetti [Italie] ; Irena Rektorova [République tchèque] ; Milica G. Kramberger [Slovénie] ; Maria Pikkarainen [Finlande] ; Walter J. Schulz-Schaeffer [Allemagne] ; Dag Aarsland [Suède] ; Per Svenningsson [Suède] ; Lucia Farotti [Italie] ; Marcel M. Verbeek [Pays-Bas] ; Michael G. Schlossmacher [Canada]Source :
- Journal of neurochemistry [ 1471-4159 ] ; 2016.
Abstract
Cerebrospinal fluid (CSF) has been extensively studied to explore biochemical alterations in subjects with neurodegenerative disorders. In Alzheimer's disease, levels of increased CSF tau protein and decreased levels of β-amyloid 1-42 (Aβ42) have been shown to correlate with brain plaque formation and tangle pathology. Intracellular Lewy inclusions containing aggregated α-synuclein (α-syn) represent a pathological hallmark of Parkinson's disease (PD). In most - but not all - studies published to date total CSF α-syn concentrations have been found to be decreased in disorders related to α-syn pathology, that is, PD, dementia with Lewy bodies and multiple system atrophy. However, these reports show extensive signal overlap among tested individuals, thereby diminishing its potential for routine use in clinical practice. To investigate potential biological (i.e., non-technical) confounders of reported CSF levels for α-syn, Aβ42, and tau in PD and related disorders, we carried out a methodical review of known factors that underlie signal variability and speculate on those that have not yet been tested. We discuss several biological factors, such as neuropathology, demographics, clinical phenotype, progression and duration of disease, concomitant illnesses and, last but not least, pharmacotherapy, which in isolation or combination can substantially alter values for CSF proteins of interest. Enhanced implementation of standardized clinical protocols, streamlined operating procedures, and further progress in the development of validated assays for CSF proteins have the potential to (i) inform us as to the pathogenesis of disease, (ii) support the laboratory-based diagnosis for symptomatic subjects in the future, and (iii) facilitate breakthrough therapies to alter the course of neurodegenerative disorders, such as PD and Alzheimer's disease. Cerebrospinal fluid (CSF) has been extensively studied to explore biochemical alterations in subjects with neurodegenerative disorders. To investigate potential biological confounders of reported CSF levels for α-synuclein (α-Syn), amyloid-β 1-42(Aβ42) and tau protein in Parkinson's disease and related disorders, we reviewed the current literature for known factors that underlie signal variability and speculate on those that have not yet been tested. This article is part of a special issue on Parkinson disease.
DOI: 10.1111/jnc.13390
PubMed: 26452984
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Kramberger</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, University Medical Center Ljubljana, Ljubljana, Slovenia.</nlm:affiliation><country xml:lang="fr">Slovénie</country><wicri:regionArea>Department of Neurology, University Medical Center Ljubljana, Ljubljana</wicri:regionArea></affiliation></author><author><name sortKey="Pikkarainen, Maria" sort="Pikkarainen, Maria" uniqKey="Pikkarainen M" first="Maria" last="Pikkarainen">Maria Pikkarainen</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Clinical Medicine / Neurology, University of Eastern Finland, Kuopio, Finland.</nlm:affiliation><country xml:lang="fr">Finlande</country><wicri:regionArea>Institute of Clinical Medicine / Neurology, University of Eastern Finland, Kuopio</wicri:regionArea></affiliation></author><author><name sortKey="Schulz Schaeffer, Walter J" sort="Schulz Schaeffer, Walter J" uniqKey="Schulz Schaeffer W" first="Walter J" last="Schulz-Schaeffer">Walter J. Schulz-Schaeffer</name><affiliation wicri:level="1"><nlm:affiliation>University Medical Center (Department of Neuropathology), Georg-August University Goettingen, Goettingen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>University Medical Center (Department of Neuropathology), Georg-August University Goettingen, Goettingen</wicri:regionArea></affiliation></author><author><name sortKey="Aarsland, Dag" sort="Aarsland, Dag" uniqKey="Aarsland D" first="Dag" last="Aarsland">Dag Aarsland</name><affiliation wicri:level="1"><nlm:affiliation>Division for Neurogeriatrics, Department of NVS, Karolinska Institutet, Center for Alzheimer Research, Stockholm, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Division for Neurogeriatrics, Department of NVS, Karolinska Institutet, Center for Alzheimer Research, Stockholm</wicri:regionArea></affiliation></author><author><name sortKey="Svenningsson, Per" sort="Svenningsson, Per" uniqKey="Svenningsson P" first="Per" last="Svenningsson">Per Svenningsson</name><affiliation wicri:level="1"><nlm:affiliation>Department for Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department for Clinical Neuroscience, Karolinska Institute, Stockholm</wicri:regionArea></affiliation></author><author><name sortKey="Farotti, Lucia" sort="Farotti, Lucia" uniqKey="Farotti L" first="Lucia" last="Farotti">Lucia Farotti</name><affiliation wicri:level="1"><nlm:affiliation>Centro Disturbi della Memoria- Unità Valutativa Alzheimer, Clinica Neurologica, Università di Perugia, Perugia, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Centro Disturbi della Memoria- Unità Valutativa Alzheimer, Clinica Neurologica, Università di Perugia, Perugia</wicri:regionArea></affiliation></author><author><name sortKey="Verbeek, Marcel M" sort="Verbeek, Marcel M" uniqKey="Verbeek M" first="Marcel M" last="Verbeek">Marcel M. Verbeek</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Department of Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, The Netherlands.</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, Department of Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen</wicri:regionArea></affiliation></author><author><name sortKey="Schlossmacher, Michael G" sort="Schlossmacher, Michael G" uniqKey="Schlossmacher M" first="Michael G" last="Schlossmacher">Michael G. Schlossmacher</name><affiliation wicri:level="1"><nlm:affiliation>Program in Neuroscience and Division of Neurology, The Ottawa Hospital, University of Ottawa Brain & Mind Research Institute, Ottawa, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Program in Neuroscience and Division of Neurology, The Ottawa Hospital, University of Ottawa Brain & Mind Research Institute, Ottawa, Ontario</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of neurochemistry</title><idno type="eISSN">1471-4159</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cerebrospinal fluid (CSF) has been extensively studied to explore biochemical alterations in subjects with neurodegenerative disorders. In Alzheimer's disease, levels of increased CSF tau protein and decreased levels of β-amyloid 1-42 (Aβ42) have been shown to correlate with brain plaque formation and tangle pathology. Intracellular Lewy inclusions containing aggregated α-synuclein (α-syn) represent a pathological hallmark of Parkinson's disease (PD). In most - but not all - studies published to date total CSF α-syn concentrations have been found to be decreased in disorders related to α-syn pathology, that is, PD, dementia with Lewy bodies and multiple system atrophy. However, these reports show extensive signal overlap among tested individuals, thereby diminishing its potential for routine use in clinical practice. To investigate potential biological (i.e., non-technical) confounders of reported CSF levels for α-syn, Aβ42, and tau in PD and related disorders, we carried out a methodical review of known factors that underlie signal variability and speculate on those that have not yet been tested. We discuss several biological factors, such as neuropathology, demographics, clinical phenotype, progression and duration of disease, concomitant illnesses and, last but not least, pharmacotherapy, which in isolation or combination can substantially alter values for CSF proteins of interest. Enhanced implementation of standardized clinical protocols, streamlined operating procedures, and further progress in the development of validated assays for CSF proteins have the potential to (i) inform us as to the pathogenesis of disease, (ii) support the laboratory-based diagnosis for symptomatic subjects in the future, and (iii) facilitate breakthrough therapies to alter the course of neurodegenerative disorders, such as PD and Alzheimer's disease. Cerebrospinal fluid (CSF) has been extensively studied to explore biochemical alterations in subjects with neurodegenerative disorders. To investigate potential biological confounders of reported CSF levels for α-synuclein (α-Syn), amyloid-β 1-42(Aβ42) and tau protein in Parkinson's disease and related disorders, we reviewed the current literature for known factors that underlie signal variability and speculate on those that have not yet been tested. This article is part of a special issue on Parkinson disease.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">26452984</PMID><DateCreated><Year>2015</Year><Month>10</Month><Day>10</Day></DateCreated><DateRevised><Year>2016</Year><Month>10</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1471-4159</ISSN><JournalIssue CitedMedium="Internet"><Volume>139 Suppl 1</Volume><PubDate><Year>2016</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Biological confounders for the values of cerebrospinal fluid proteins in Parkinson's disease and related disorders.</ArticleTitle><Pagination><MedlinePgn>290-317</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jnc.13390</ELocationID><Abstract><AbstractText>Cerebrospinal fluid (CSF) has been extensively studied to explore biochemical alterations in subjects with neurodegenerative disorders. In Alzheimer's disease, levels of increased CSF tau protein and decreased levels of β-amyloid 1-42 (Aβ42) have been shown to correlate with brain plaque formation and tangle pathology. Intracellular Lewy inclusions containing aggregated α-synuclein (α-syn) represent a pathological hallmark of Parkinson's disease (PD). In most - but not all - studies published to date total CSF α-syn concentrations have been found to be decreased in disorders related to α-syn pathology, that is, PD, dementia with Lewy bodies and multiple system atrophy. However, these reports show extensive signal overlap among tested individuals, thereby diminishing its potential for routine use in clinical practice. To investigate potential biological (i.e., non-technical) confounders of reported CSF levels for α-syn, Aβ42, and tau in PD and related disorders, we carried out a methodical review of known factors that underlie signal variability and speculate on those that have not yet been tested. We discuss several biological factors, such as neuropathology, demographics, clinical phenotype, progression and duration of disease, concomitant illnesses and, last but not least, pharmacotherapy, which in isolation or combination can substantially alter values for CSF proteins of interest. Enhanced implementation of standardized clinical protocols, streamlined operating procedures, and further progress in the development of validated assays for CSF proteins have the potential to (i) inform us as to the pathogenesis of disease, (ii) support the laboratory-based diagnosis for symptomatic subjects in the future, and (iii) facilitate breakthrough therapies to alter the course of neurodegenerative disorders, such as PD and Alzheimer's disease. Cerebrospinal fluid (CSF) has been extensively studied to explore biochemical alterations in subjects with neurodegenerative disorders. To investigate potential biological confounders of reported CSF levels for α-synuclein (α-Syn), amyloid-β 1-42(Aβ42) and tau protein in Parkinson's disease and related disorders, we reviewed the current literature for known factors that underlie signal variability and speculate on those that have not yet been tested. This article is part of a special issue on Parkinson disease.</AbstractText><CopyrightInformation>© 2016 International Society for Neurochemistry.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mollenhauer</LastName><ForeName>Brit</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Paracelsus-Elena-Klinik, Kassel, Germany. brit.mollenhauer@paracelsus-kliniken.de.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>University Medical Center (Department of Neuropathology), Georg-August University Goettingen, Goettingen, Germany. brit.mollenhauer@paracelsus-kliniken.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parnetti</LastName><ForeName>Lucilla</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Centro Disturbi della Memoria- Unità Valutativa Alzheimer, Clinica Neurologica, Università di Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rektorova</LastName><ForeName>Irena</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Applied Neuroscience Group, CEITEC MU, Masaryk University, Brno, Czech Republic.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kramberger</LastName><ForeName>Milica G</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>Department of Neurology, University Medical Center Ljubljana, Ljubljana, Slovenia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Division for Neurogeriatrics, Department of NVS, Karolinska Institutet, Center for Alzheimer Research, Stockholm, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pikkarainen</LastName><ForeName>Maria</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute of Clinical Medicine / Neurology, University of Eastern Finland, Kuopio, Finland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schulz-Schaeffer</LastName><ForeName>Walter J</ForeName><Initials>WJ</Initials><AffiliationInfo><Affiliation>University Medical Center (Department of Neuropathology), Georg-August University Goettingen, Goettingen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aarsland</LastName><ForeName>Dag</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Division for Neurogeriatrics, Department of NVS, Karolinska Institutet, Center for Alzheimer Research, Stockholm, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Svenningsson</LastName><ForeName>Per</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department for Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Farotti</LastName><ForeName>Lucia</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Centro Disturbi della Memoria- Unità Valutativa Alzheimer, Clinica Neurologica, Università di Perugia, Perugia, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Verbeek</LastName><ForeName>Marcel M</ForeName><Initials>MM</Initials><AffiliationInfo><Affiliation>Department of Neurology, Department of Laboratory Medicine, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schlossmacher</LastName><ForeName>Michael G</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>Program in Neuroscience and Division of Neurology, The Ottawa Hospital, University of Ottawa Brain & Mind Research Institute, Ottawa, Ontario, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>02</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">cerebrospinal fluid biomarker</Keyword><Keyword MajorTopicYN="N">confounding</Keyword><Keyword MajorTopicYN="N">dementia</Keyword><Keyword MajorTopicYN="N">factors</Keyword><Keyword MajorTopicYN="N">neuropathology</Keyword><Keyword MajorTopicYN="N">tau-protein</Keyword><Keyword MajorTopicYN="N">α-synuclein</Keyword><Keyword MajorTopicYN="N">β-amyloid</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>02</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>09</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>09</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>10</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>10</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>10</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26452984</ArticleId><ArticleId IdType="doi">10.1111/jnc.13390</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour 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