Saliva Neurofilament Light Chain Is Not a Diagnostic Biomarker for Neurodegeneration in a Mixed Memory Clinic Population

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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.

OriginalsprogEngelsk
Artikelnummer659898
TidsskriftFrontiers in Aging Neuroscience
Vol/bind13
ISSN1663-4365
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
The authors are grateful to all the clinical personnel at the Copenhagen Memory Clinic, Copenhagen University Hospital, Rigshospitalet and the Regional Dementia Research Center, Zealand University Hospital, Roskilde. Funding. This research was funded by the Lundbeck Foundation, Grosserer L. F. Fights Foundation, Augustinus Foundation, Frimodt-Heineke Foundation, and the Foundation for Neurological Research. The Danish Dementia Biobank (DDBB) was supported by the Absalon Foundation of 1st May 1978 and Simon Spies Foundation. KB was supported by the Swedish Research Council (#2017-00915), the Alzheimer Drug Discovery Foundation (ADDF), United States (#RDAPB-201809-2016615), the Swedish Alzheimer Foundation (#AF-742881), Hj?rnfonden, Sweden (#FO2017-0243), the Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement (#ALFGBG-715986), the European Union Joint Program for Neurodegenerative Disorders (JPND2019-466-236), and the National Institutes of Health (NIH), United States (grant #1R01AG068398-01). HZ was a Wallenberg Scholar supported by grants from the Swedish Research Council (#2018-02532), the European Research Council (#681712), Swedish State Support for Clinical Research (#ALFGBG-720931), the Alzheimer Drug Discovery Foundation (ADDF), United States (#201809-2016862), the AD Strategic Fund and the Alzheimer?s Association (#ADSF-21-831376-C, #ADSF-21-831381-C, and #ADSF-21-831377-C), the Olav Thon Foundation, the Erling-Persson Family Foundation, Stiftelsen f?r Gamla Tj?narinnor, Hj?rnfonden, Sweden (#FO2019-0228), the European Union?s Horizon 2020 Research and Innovation Program under the Marie Sk?odowska-Curie grant agreement No. 860197 (MIRIADE), and the UK Dementia Research Institute at UCL.

Publisher Copyright:
© Copyright © 2021 Gleerup, Sanna, Høgh, Simrén, Blennow, Zetterberg, Hasselbalch, Ashton and Simonsen.

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