Biological confounders for the values of cerebrospinal fluid proteins in Parkinson's disease and related disorders

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 format...

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Published inJournal of neurochemistry Vol. 139; no. S1; pp. 290 - 317
Main Authors Mollenhauer, Brit, Parnetti, Lucilla, Rektorova, Irena, Kramberger, Milica G., Pikkarainen, Maria, Schulz‐Schaeffer, Walter J., Aarsland, Dag, Svenningsson, Per, Farotti, Lucia, Verbeek, Marcel M., Schlossmacher, Michael G.
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.10.2016
Subjects
alpha-Synuclein - cerebrospinal fluid
Alzheimer's disease
Amyloid beta-Peptides - cerebrospinal fluid
Animals
Biomarkers - cerebrospinal fluid
cerebrospinal fluid biomarker
Cerebrospinal Fluid Proteins - cerebrospinal fluid
Clinical Trials as Topic - methods
Cognition Disorders - cerebrospinal fluid
Cognition Disorders - diagnosis
confounding
dementia
factors
Humans
neuropathology
Parkinson Disease - cerebrospinal fluid
Parkinson Disease - diagnosis
Parkinson's disease
Pathology
Peptide Fragments - cerebrospinal fluid
Proteins
tau Proteins - cerebrospinal fluid
tau‐protein
α‐synuclein
β‐amyloid
confounding
Parkinson's disease
cerebrospinal fluid biomarker
dementia
tau-protein
neuropathology
α-synuclein
factors
β-amyloid
Online AccessGet full text
ISSN0022-3042
1471-4159
DOI10.1111/jnc.13390

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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. 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.
AbstractList 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. 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.
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.
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 [beta]-amyloid 1-42 (A[beta]42) have been shown to correlate with brain plaque formation and tangle pathology. Intracellular Lewy inclusions containing aggregated [alpha]-synuclein ([alpha]-syn) represent a pathological hallmark of Parkinson's disease (PD). In most - but not all - studies published to date total CSF [alpha]-syn concentrations have been found to be decreased in disorders related to [alpha]-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 [alpha]-syn, A[beta]42, 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 [alpha]-synuclein ([alpha]-Syn), amyloid-[beta] 1-42(A[beta]42) 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 aspecial issue on Parkinson disease.
Author Aarsland, Dag
Verbeek, Marcel M.
Schulz‐Schaeffer, Walter J.
Parnetti, Lucilla
Rektorova, Irena
Mollenhauer, Brit
Farotti, Lucia
Pikkarainen, Maria
Svenningsson, Per
Schlossmacher, Michael G.
Kramberger, Milica G.
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  organization: University of Ottawa Brain & Mind Research Institute
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2016 International Society for Neurochemistry.
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Issue S1
Keywords confounding
Parkinson's disease
cerebrospinal fluid biomarker
dementia
tau-protein
neuropathology
α-synuclein
factors
β-amyloid
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
2016 International Society for Neurochemistry.
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Publisher Blackwell Publishing Ltd
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Snippet Cerebrospinal fluid (CSF) has been extensively studied to explore biochemical alterations in subjects with neurodegenerative disorders. In Alzheimer's disease,...
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SubjectTerms alpha-Synuclein - cerebrospinal fluid
Alzheimer's disease
Amyloid beta-Peptides - cerebrospinal fluid
Animals
Biomarkers - cerebrospinal fluid
cerebrospinal fluid biomarker
Cerebrospinal Fluid Proteins - cerebrospinal fluid
Clinical Trials as Topic - methods
Cognition Disorders - cerebrospinal fluid
Cognition Disorders - diagnosis
confounding
dementia
factors
Humans
neuropathology
Parkinson Disease - cerebrospinal fluid
Parkinson Disease - diagnosis
Parkinson's disease
Pathology
Peptide Fragments - cerebrospinal fluid
Proteins
tau Proteins - cerebrospinal fluid
tau‐protein
α‐synuclein
β‐amyloid
Title Biological confounders for the values of cerebrospinal fluid proteins in Parkinson's disease and related disorders
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjnc.13390
https://www.ncbi.nlm.nih.gov/pubmed/26452984
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Volume 139
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