Evidence map›Paper›PMID 31182505›Full record

ArticleNeurology2019

Plasma and CSF neurofilament light: Relation to longitudinal neuroimaging and cognitive measures.

Michelle M Mielke, Jeremy A Syrjanen, Kaj Blennow, Henrik Zetterberg, Prashanthi Vemuri, Ingmar Skoog, Mary M Machulda, Walter K Kremers, David S Knopman, Clifford Jack and 2 more

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Article in Neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
186citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

186 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  17. Diabetes, hyperglycemia, and ATN blood biomarkers in Hispanic/Latino populations: SOL-INCA study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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126 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Michelle M MielkeFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK. mielke.michelle@mayo.edu.
Jeremy A SyrjanenFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Kaj BlennowFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Henrik ZetterbergFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Prashanthi VemuriFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Ingmar SkoogFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Mary M MachuldaFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Walter K KremersFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
David S KnopmanFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Clifford JackFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Ronald C PetersenFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
Silke KernFrom the Departments of Health Sciences Research (M.M. Mielke, J.A.S., W.K.K., R.C.P., S.K.), Neurology (M.M. Mielke, D.S.K., R.C.P.), Radiology (P.V., C.J.), and Psychiatry and Psychology (M.M. Machulda), Mayo Clinic, Rochester, MN; Department of Psychiatry and Neurochemistry (K.B., H.Z., I.S., S.K.), Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg; Clinical Neurochemistry Laboratory (K.B., H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Institute of Neurology (H.Z.), University College London, Queen Square; and UK Dementia Research Institute at UCL (H.Z.), London, UK.

Funding

SUPPLEMENT TO ALZHEIMERS DISEASE PATIENT REGISTRYU01AG006786 · NIA · MAYO CLINIC ROCHESTER · PI GRAFF-RADFORD, JONATHAN, JACK, CLIFFORD R. · 1986 to 2023
$49.6M
PREDICTING ALZHEIMERS DISEASE WITH MAGNETIC RESONANCER01AG011378 · NIA · MAYO CLINIC ROCHESTER · PI JACK, CLIFFORD R. · 1993 to 2017
$12.1M
Disease pathways in the population determined by amyloid, tau, and neurodegeneration imaging biomarkersR37AG011378 · NIA · MAYO CLINIC ROCHESTER · PI CLIFFORD R. JACK · 2018 to 2026
$6.8M
Validating the New Criteria for Preclinical Alzheimer's diseaseR01AG041851 · NIA · MAYO CLINIC ROCHESTER · PI JACK, CLIFFORD R., KNOPMAN, DAVID S · 2012 to 2021
$6.3M
Development, Validation, and Application of an Imaging based CVD ScaleR01NS097495 · NINDS · MAYO CLINIC ROCHESTER · PI VEMURI, PRASHANTHI · 2016 to 2020
$2.9M
Sphingolipids and Inflammation in the Development and Progression of Alzheimer'sR01AG049704 · NIA · MAYO CLINIC ROCHESTER · PI MIELKE, MICHELLE M · 2015 to 2018
$1.5M
NIA NIH HHS R01 AG011378NIA NIH HHS R01 AG041851NIA NIH HHS R01 AG049704NIA NIH HHS R37 AG011378NIA NIH HHS U01 AG006786NINDS NIH HHS R01 NS097495
6 · The paper itself

Abstract

objectiveWe aimed to (1) assess and compare baseline plasma and CSF neurofilament light (NfL) for cross-sectional and longitudinal associations with neuroimaging or cognition and (2) determine whether change in plasma NfL corresponded with change in these outcomes.

methodsSeventy-nine participants without dementia, median age 76 years, had plasma and CSF NfL, neuropsychological testing, and neuroimaging (MRI, amyloid PET, FDG-PET) at the same study visit, and a repeat visit (15 or 30 months later) with both plasma NfL and neuroimaging. Plasma NfL was measured on the Simoa-HD1 Platform and CSF NfL with an in-house ELISA. Linear mixed effects models were used to examine the associations between baseline plasma or CSF NfL and cognitive and neuroimaging outcomes adjusting for age, sex, and education. The relationship between change in plasma NfL and change in the outcomes was assessed using linear regression.

resultsThere were no cross-sectional associations between CSF or plasma NfL and any neuroimaging or cognitive measure. Longitudinally, higher baseline plasma NfL was associated with worsening in all neuroimaging measures, except amyloid PET, and global cognition. Higher baseline CSF NfL was associated with worsening in cortical thickness and diffusion MRI. The beta estimates for CSF NfL were similar to those for plasma NfL. Change in plasma NfL was associated with change in global cognition, attention, and amyloid PET.

conclusionElevated baseline plasma NfL is a prognostic marker of cognitive decline and neuroimaging measures of neurodegeneration, and has similar effect sizes to baseline CSF NfL. Change in plasma NfL also tracked with short-term cognitive change.

Indexed as

CognitionAgedAniline CompoundsAttentionBrainCognitive DysfunctionFemaleFluorodeoxyglucose F18HumansLinear ModelsLongitudinal StudiesMagnetic Resonance ImagingMaleNeurofilament ProteinsNeuropsychological TestsPositron-Emission Tomography2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazoleAniline CompoundsFluorodeoxyglucose F18neurofilament protein LNeurofilament ProteinsRadiopharmaceuticalsThiazoles

Identifiers

PMID31182505
PMCPMC6656645

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.