Saliva Neurofilament Light Chain Is Not a Diagnostic Biomarker for Neurodegeneration in a Mixed Memory Clinic Population
Neurodegeneration and axonal injury result in an increasing release of neurofilament light chain (NfL) into bodily fluids, including cerebrospinal fluid (CSF) and blood. Numerous studies have shown that NfL levels in CSF and blood are increased in neurodegenerative disorders and monitor neurodegener...
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| Published in: | Frontiers in aging neuroscience Vol. 13; p. 659898 |
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| Format: | Journal Article |
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| Abstract | Neurodegeneration and axonal injury result in an increasing release of neurofilament light chain (NfL) into bodily fluids, including cerebrospinal fluid (CSF) and blood. Numerous studies have shown that NfL levels in CSF and blood are increased in neurodegenerative disorders and monitor neurodegeneration. Saliva is an easily accessible biofluid that could be utilized as a biofluid measurement of Alzheimer's disease (AD) biomarkers. In this study, for the first time, salivary NfL was measured and compared to plasma NfL in a consecutive cohort of patients referred to cognitive assessments. In two mixed memory clinic cohorts, saliva samples were taken from 152 patients, AD (
= 49), mild cognitive impairment (MCI) (
= 47), non-AD (
= 56), and also 17 healthy controls. In addition, 135 also had a matching plasma sample. All saliva and plasma samples were analyzed for NfL, and the association between saliva and plasma NfL and CSF levels of total tau (t-tau), phosphorylated tau (p-tau), and beta amyloid 1-42 (Aβ42) were investigated. In total, 162/169 had quantifiable levels of salivary NfL by single molecule array (Simoa). No statistically significant differences were found in salivary NfL concentration across the diagnostic groups, but as expected, significant increases were found for plasma NfL in dementia cases (
< 0.0001). There was no association between saliva and plasma NfL levels. Furthermore, saliva NfL did not correlate with CSF Aβ42, p-tau, or tau concentrations. In conclusion, NfL is detectable in saliva but does not reflect neurodegeneration in the brain. |
|---|---|
| AbstractList | Neurodegeneration and axonal injury result in an increasing release of neurofilament light chain (NfL) into bodily fluids, including cerebrospinal fluid (CSF) and blood. Numerous studies have shown that NfL levels in CSF and blood are increased in neurodegenerative disorders and monitor neurodegeneration. Saliva is an easily accessible biofluid that could be utilized as a biofluid measurement of Alzheimer's disease (AD) biomarkers. In this study, for the first time, salivary NfL was measured and compared to plasma NfL in a consecutive cohort of patients referred to cognitive assessments. In two mixed memory clinic cohorts, saliva samples were taken from 152 patients, AD (
= 49), mild cognitive impairment (MCI) (
= 47), non-AD (
= 56), and also 17 healthy controls. In addition, 135 also had a matching plasma sample. All saliva and plasma samples were analyzed for NfL, and the association between saliva and plasma NfL and CSF levels of total tau (t-tau), phosphorylated tau (p-tau), and beta amyloid 1-42 (Aβ42) were investigated. In total, 162/169 had quantifiable levels of salivary NfL by single molecule array (Simoa). No statistically significant differences were found in salivary NfL concentration across the diagnostic groups, but as expected, significant increases were found for plasma NfL in dementia cases (
< 0.0001). There was no association between saliva and plasma NfL levels. Furthermore, saliva NfL did not correlate with CSF Aβ42, p-tau, or tau concentrations. In conclusion, NfL is detectable in saliva but does not reflect neurodegeneration in the brain. Neurodegeneration and axonal injury result in an increasing release of neurofilament light chain (NfL) into bodily fluids, including cerebrospinal fluid (CSF) and blood. Numerous studies have shown that NfL levels in CSF and blood are increased in neurodegenerative disorders and monitor neurodegeneration. Saliva is an easily accessible biofluid that could be utilized as a biofluid measurement of Alzheimer's disease (AD) biomarkers. In this study, for the first time, salivary NfL was measured and compared to plasma NfL in a consecutive cohort of patients referred to cognitive assessments. In two mixed memory clinic cohorts, saliva samples were taken from 152 patients, AD (n = 49), mild cognitive impairment (MCI) (n = 47), non-AD (n = 56), and also 17 healthy controls. In addition, 135 also had a matching plasma sample. All saliva and plasma samples were analyzed for NfL, and the association between saliva and plasma NfL and CSF levels of total tau (t-tau), phosphorylated tau (p-tau), and beta amyloid 1-42 (Aβ42) were investigated. In total, 162/169 had quantifiable levels of salivary NfL by single molecule array (Simoa). No statistically significant differences were found in salivary NfL concentration across the diagnostic groups, but as expected, significant increases were found for plasma NfL in dementia cases (P < 0.0001). There was no association between saliva and plasma NfL levels. Furthermore, saliva NfL did not correlate with CSF Aβ42, p-tau, or tau concentrations. In conclusion, NfL is detectable in saliva but does not reflect neurodegeneration in the brain. Neurodegeneration and axonal injury result in an increasing release of neurofilament light chain (NfL) into bodily fluids, including cerebrospinal fluid (CSF) and blood. Numerous studies have shown that NfL levels in CSF and blood are increased in neurodegenerative disorders and monitor neurodegeneration. Saliva is an easily accessible biofluid that could be utilized as a biofluid measurement of Alzheimer's disease (AD) biomarkers. In this study, for the first time, salivary NfL was measured and compared to plasma NfL in a consecutive cohort of patients referred to cognitive assessments. In two mixed memory clinic cohorts, saliva samples were taken from 152 patients, AD (n = 49), mild cognitive impairment (MCI) (n = 47), non-AD (n = 56), and also 17 healthy controls. In addition, 135 also had a matching plasma sample. All saliva and plasma samples were analyzed for NfL, and the association between saliva and plasma NfL and CSF levels of total tau (t-tau), phosphorylated tau (p-tau), and beta amyloid 1-42 (A beta 42) were investigated. In total, 162/169 had quantifiable levels of salivary NfL by single molecule array (Simoa). No statistically significant differences were found in salivary NfL concentration across the diagnostic groups, but as expected, significant increases were found for plasma NfL in dementia cases (P < 0.0001). There was no association between saliva and plasma NfL levels. Furthermore, saliva NfL did not correlate with CSF A beta 42, p-tau, or tau concentrations. In conclusion, NfL is detectable in saliva but does not reflect neurodegeneration in the brain. Neurodegeneration and axonal injury result in an increasing release of neurofilament light chain (NfL) into bodily fluids, including cerebrospinal fluid (CSF) and blood. Numerous studies have shown that NfL levels in CSF and blood are increased in neurodegenerative disorders and monitor neurodegeneration. Saliva is an easily accessible biofluid that could be utilized as a biofluid measurement of Alzheimer’s disease (AD) biomarkers. In this study, for the first time, salivary NfL was measured and compared to plasma NfL in a consecutive cohort of patients referred to cognitive assessments. In two mixed memory clinic cohorts, saliva samples were taken from 152 patients, AD ( n = 49), mild cognitive impairment (MCI) ( n = 47), non-AD ( n = 56), and also 17 healthy controls. In addition, 135 also had a matching plasma sample. All saliva and plasma samples were analyzed for NfL, and the association between saliva and plasma NfL and CSF levels of total tau (t-tau), phosphorylated tau (p-tau), and beta amyloid 1–42 (Aβ42) were investigated. In total, 162/169 had quantifiable levels of salivary NfL by single molecule array (Simoa). No statistically significant differences were found in salivary NfL concentration across the diagnostic groups, but as expected, significant increases were found for plasma NfL in dementia cases ( P < 0.0001). There was no association between saliva and plasma NfL levels. Furthermore, saliva NfL did not correlate with CSF Aβ42, p-tau, or tau concentrations. In conclusion, NfL is detectable in saliva but does not reflect neurodegeneration in the brain. Neurodegenerative disorders are an increasing concern, and consequently non-invasive biomarkers are needed. Neurodegeneration leads to an increasing release of the neuron-specific neurofilament light chain (NfL) protein into body fluids, including cerebrospinal fluid (CSF) and blood. Numerous studies have shown that NfL levels in CSF and blood can monitor neurodegeneration. Saliva has been suggested to be a candidate biofluid for the measurement of biomarkers for Alzheimer’s disease (AD). In this study, salivary NfL was for the first time measured and compared to plasma NfL in consecutive a cohort of patients referred to cognitive assessments. From two mixed, memory clinic cohorts, 152 consecutive patients and 17 healthy controls were recruited. Of these, 135 also had a matching plasma sample. All saliva and plasma samples were analyzed for NfL, and the association between saliva and plasma NfL, and CSF levels of total tau (t-tau), phosphorylated tau (p-tau), and beta amyloid 1-42 (A42) were investigated. In total, 162/169 had quantifiable levels of salivary NfL by single molecule array (Simoa). No statistically significant differences were found in salivary NfL concentration across the diagnostic groups, but as expected, significant increases were found for plasma NfL in dementia cases (P=<0.0001). There was no association between saliva and plasma NfL levels. Furthermore, saliva NfL did not correlate with CSF A42, p-tau or tau concentrations. Although NfL in saliva was quantifiable, it did not correlate with plasma NfL and was not useful to detect AD or other dementias. Saliva NfL concentration does not reflect neurodegeneration in the brain. |
| Author | Hasselbalch, Steen Gregers Gleerup, Helena Sophia Blennow, Kaj Zetterberg, Henrik Sanna, Federica Høgh, Peter Simonsen, Anja Hviid Simrén, Joel Ashton, Nicholas J |
| AuthorAffiliation | 6 Department of Neurodegenerative Disease, UCL Institute of Neurology , London , United Kingdom 9 King’s College London, Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Institute Clinical Neuroscience Institute , London , United Kingdom 3 Regional Dementia Research Centre, Department of Neurology, Zealand University Hospital , Roskilde , Denmark 10 NIHR Biomedical Research Centre for Mental Health and Biomedical Research Unit for Dementia at South London and Maudsley NHS Foundation , London , United Kingdom 8 Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg , Gothenburg , Sweden 5 Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital , Mölndal , Sweden 2 Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg , Mölndal , Sweden 7 UK Dementia Research Institute at UCL , London , United Kingdom 1 Department of Neurology, Danish Dementia Resea |
| AuthorAffiliation_xml | – name: 2 Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg , Mölndal , Sweden – name: 6 Department of Neurodegenerative Disease, UCL Institute of Neurology , London , United Kingdom – name: 10 NIHR Biomedical Research Centre for Mental Health and Biomedical Research Unit for Dementia at South London and Maudsley NHS Foundation , London , United Kingdom – name: 4 Department of Clinical Medicine, Faculty of Health and Medical Science, University of Copenhagen , Copenhagen , Denmark – name: 9 King’s College London, Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Institute Clinical Neuroscience Institute , London , United Kingdom – name: 5 Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital , Mölndal , Sweden – name: 3 Regional Dementia Research Centre, Department of Neurology, Zealand University Hospital , Roskilde , Denmark – name: 7 UK Dementia Research Institute at UCL , London , United Kingdom – name: 8 Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg , Gothenburg , Sweden – name: 1 Department of Neurology, Danish Dementia Research Centre, Copenhagen University Hospital , Copenhagen , Denmark |
| Author_xml | – sequence: 1 givenname: Helena Sophia surname: Gleerup fullname: Gleerup, Helena Sophia organization: Department of Neurology, Danish Dementia Research Centre, Copenhagen University Hospital, Copenhagen, Denmark – sequence: 2 givenname: Federica surname: Sanna fullname: Sanna, Federica organization: Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden – sequence: 3 givenname: Peter surname: Høgh fullname: Høgh, Peter organization: Department of Clinical Medicine, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark – sequence: 4 givenname: Joel surname: Simrén fullname: Simrén, Joel organization: Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden – sequence: 5 givenname: Kaj surname: Blennow fullname: Blennow, Kaj organization: Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden – sequence: 6 givenname: Henrik surname: Zetterberg fullname: Zetterberg, Henrik organization: UK Dementia Research Institute at UCL, London, United Kingdom – sequence: 7 givenname: Steen Gregers surname: Hasselbalch fullname: Hasselbalch, Steen Gregers organization: Department of Clinical Medicine, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark – sequence: 8 givenname: Nicholas J surname: Ashton fullname: Ashton, Nicholas J organization: NIHR Biomedical Research Centre for Mental Health and Biomedical Research Unit for Dementia at South London and Maudsley NHS Foundation, London, United Kingdom – sequence: 9 givenname: Anja Hviid surname: Simonsen fullname: Simonsen, Anja Hviid organization: Department of Neurology, Danish Dementia Research Centre, Copenhagen University Hospital, Copenhagen, Denmark |
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| Copyright | Copyright © 2021 Gleerup, Sanna, Høgh, Simrén, Blennow, Zetterberg, Hasselbalch, Ashton and Simonsen. 2021. 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. Copyright © 2021 Gleerup, Sanna, Høgh, Simrén, Blennow, Zetterberg, Hasselbalch, Ashton and Simonsen. 2021 Gleerup, Sanna, Høgh, Simrén, Blennow, Zetterberg, Hasselbalch, Ashton and Simonsen |
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| Keywords | saliva neurofilament light chain Alzheimer’s disease neurodegeneration dementia biomarker plasma |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors have contributed equally to this work Reviewed by: Avijit Banik, Emory University, United States; H. Bea Kuiperij, Radboud University Nijmegen Medical Centre, Netherlands Edited by: Ramesh Kandimalla, Indian Institute of Chemical Technology (CSIR), India |
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| Snippet | Neurodegeneration and axonal injury result in an increasing release of neurofilament light chain (NfL) into bodily fluids, including cerebrospinal fluid (CSF)... Neurodegenerative disorders are an increasing concern, and consequently non-invasive biomarkers are needed. Neurodegeneration leads to an increasing release of... |
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| Title | Saliva Neurofilament Light Chain Is Not a Diagnostic Biomarker for Neurodegeneration in a Mixed Memory Clinic Population |
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