Evidence map›Paper›PMID 39054505›Full record

ArticleAlzheimer's research & therapy2024

Plasma neurofilament light, glial fibrillary acid protein, and phosphorylated tau 181 as biomarkers for neuropsychiatric symptoms and related clinical disease progression.

Miriam Rabl, Leonardo Zullo, Piotr Lewczuk, Johannes Kornhuber, Thomas K Karikari, Kaj Blennow, Henrik Zetterberg, Francesco Bavato, Boris B Quednow, Erich Seifritz and 3 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Miriam RablDepartment of Adult Psychiatry and Psychotherapy, University Hospital of Psychiatry Zurich, University of Zurich, Lenggstrasse 31, Zurich, 8032, Switzerland. miriam.rabl@bli.uzh.ch.
Leonardo ZulloOld-Age Psychiatry Service, Department of Psychiatry, Lausanne University Hospital, Lausanne, 1005, Switzerland.
Piotr LewczukDepartment of Psychiatry and Psychotherapy, Universitätsklinikum Erlangen and Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Johannes KornhuberDepartment of Psychiatry and Psychotherapy, Universitätsklinikum Erlangen and Friedrich-Alexander Universität Erlangen-Nürnberg, 91054, Erlangen, Germany.
Thomas K KarikariDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, 431 41, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, 431 41, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, 431 41, Sweden.
Francesco BavatoDepartment of Adult Psychiatry and Psychotherapy, University Hospital of Psychiatry Zurich, University of Zurich, Lenggstrasse 31, Zurich, 8032, Switzerland.
Boris B QuednowExperimental and Clinical Pharmacopsychology, Department of Adult Psychiatry and Psychotherapy, University Hospital of Psychiatry Zurich, University of Zurich, Zurich, 8032, Switzerland.
Erich SeifritzDepartment of Adult Psychiatry and Psychotherapy, University Hospital of Psychiatry Zurich, University of Zurich, Lenggstrasse 31, Zurich, 8032, Switzerland.
Armin von GuntenOld-Age Psychiatry Service, Department of Psychiatry, Lausanne University Hospital, Lausanne, 1005, Switzerland.
Christopher ClarkDepartment of Adult Psychiatry and Psychotherapy, University Hospital of Psychiatry Zurich, University of Zurich, Lenggstrasse 31, Zurich, 8032, Switzerland.
Julius PoppDepartment of Adult Psychiatry and Psychotherapy, University Hospital of Psychiatry Zurich, University of Zurich, Lenggstrasse 31, Zurich, 8032, Switzerland.

Funding

Plasma brain-derived tau: a novel Alzheimer’s disease-type neurodegeneration biomarker with potential to complete the AT(N) scheme in bloodR01AG083874 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Thomas K Karikari · 2023 to 2026
$14.5M
Alzheimer Diagnosis in older Adults with Chronic Conditions ADACC NetworkU24AG082930 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Nicole R. Fowler, Thomas K Karikari · 2023 to 2026
$7.3M
The effects of iron on oxidative stress and Alzheimer's biomarkers in amyloid-positive and negative elderly normalR01AG068398 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHIANG, GLORIA CHIA-YI · 2020 to 2024
$2.8M
NIA NIH HHS R01 AG068398NIA NIH HHS R01 AG083874Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 320030_141179Synapsis Foundation - Dementia Research Switzerland 2017-PI01
6 · The paper itself

Abstract

backgroundNeuropsychiatric symptoms (NPS) are common in older people, may occur early in the development of dementia disorders, and have been associated with faster cognitive decline. Here, our objectives were to investigate whether plasma levels of neurofilament light chain (NfL), glial fibrillary acid protein (GFAP), and tau phosphorylated at threonine 181 (pTau181) are associated with current NPS and predict future NPS in non-demented older people. Furthermore, we tested whether the presence of NPS combined with plasma biomarkers are useful to predict Alzheimer's disease (AD) pathology and cognitive decline.

methodsOne hundred and fifty-one participants with normal cognition (n = 76) or mild cognitive impairment (n = 75) were examined in a longitudinal brain aging study at the Memory Centers, University Hospital of Lausanne, Switzerland. Plasma levels of NfL, GFAP, and pTau181 along with CSF biomarkers of AD pathology were measured at baseline. NPS were assessed through the Neuropsychiatric Inventory Questionnaire (NPI-Q), along with the cognitive and functional performance at baseline and follow-up (mean: 20 months). Different regression and ROC analyses were used to address the associations of interest.

resultsNone of the three plasma biomarker was associated with NPS at baseline. Higher GFAP levels were associated with the presence of NPS at follow-up (OR = 2.8, p = .002) and both, higher NfL and higher GFAP with an increase in the NPI-Q severity score over time (β = 0.25, p = .034 and β = 0.30, p = .013, respectively). Adding NPS and the plasma biomarkers to a reference model improved the prediction of future NPS (AUC 0.72 to 0.88, p = .002) and AD pathology (AUC 0.78 to 0.87, p = .010), but not of cognitive decline (AUC 0.79 to 0.85, p = .081).

conclusionPlasma NfL and GFAP are both associated with future NPS and NPS severity change. Considering the presence of NPS along with blood-based AD-biomarkers may improve the prediction of clinical progression of NPS over time and inform clinical decision-making in non-demented older people.

Indexed as

Alzheimer DiseaseBiomarkersCognitive DysfunctionDisease ProgressionGlial Fibrillary Acidic ProteinNeurofilament Proteinstau ProteinsAgedAged, 80 and overFemaleHumansLongitudinal StudiesMaleMiddle AgedNeuropsychological TestsPhosphorylationBiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinMAPT protein, humanneurofilament protein LNeurofilament Proteinstau ProteinsAlzheimer’s diseaseBlood-based biomarkersCognitionGFAPGlial fibrillary acid proteinNeurofilament light chainNeuropsychiatric symptomsNfLPhosphorylated tau 181pTau181

Identifiers

PMID39054505
PMCPMC11270946

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.