Evidence map›Paper›PMID 36446595›Full record

ArticleNeurology2023

Longitudinal Changes in Blood Biomarkers of Clinical Alzheimer Disease in a Biracial Population Sample.

Kumar B Rajan, Elizabeth A McAninch, Neelum T Aggarwal, Lisa L Barnes, Robert S Wilson, Jennifer Weuve, Charles S DeCarli, Denis A Evans

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 8% of its field
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Kumar B RajanFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis. kbrajan@ucdavis.edu.
Elizabeth A McAninchFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis.
Neelum T AggarwalFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis.ORCID 0000-0002-4341-8023
Lisa L BarnesFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis.
Robert S WilsonFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis.
Jennifer WeuveFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis.
Charles S DeCarliFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis.
Denis A EvansFrom the Rush Institute for Healthy Aging (K.R., D.E.), Rush University Medical Center, Chicago IL; Stanford University (E.A.M.), Palo Alto, CA; Rush Alzheimer's Disease Center (N.A., L.L.B., R.W.), Chicago IL; Boston University (J.W.), Boston, MA; and Department of Neurology (C.S.D.), University of California, Davis.
Rush University Medical Center · US

Funding

Impact of Neuroinflammation on AD Occurrence: A Bi-Generational Population StudyR01AG073627 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI NEELUM T. AGGARWAL, DENIS A EVANS · 2021 to 2026
$14.0M
Preserving Cognitive Resilience: A Biracial Parent-Offspring Study (18-4674) - Feasibility StudyR01AG058679 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI EVANS, DENIS A, RAJAN, KUMAR B. · 2019 to 2024
$13.8M
Factors Influencing Decline in AD Trends in a Biracial Population StudyRF1AG057532 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI RAJAN, KUMAR B. · 2017 to 2017
$1.7M
Nonlinear Models of Cognition Preceding AD in a Biracial Population SampleR01AG051635 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI RAJAN, KUMAR B. · 2016 to 2020
$1.5M
NIA NIH HHS R01 AG051635NIA NIH HHS R01 AG058679NIA NIH HHS R01 AG073627NIA NIH HHS RF1 AG057532
6 · The paper itself

Abstract

BACKGROUND AND

objectivesRecent studies suggest the utility of blood biomarkers in detecting changes in neurodegenerative disorders. The objective of our research was to test the hypothesis that the longitudinal changes in total tau (t-tau), neurofilament light chain (Nf-L), and glial fibrillary acidic protein (GFAP) are associated with structural MRI and the development of clinical Alzheimer disease (AD) and cognitive decline.

methodsData came from a population-based sample with serum concentrations of t-tau, Nf-L, and GFAP and cognitive characteristics measured over 17 years. The inclusion criteria for this investigation were based on participants with blood samples, cognitive function testing, and clinical diagnosis for AD. The longitudinal changes in the serum biomarkers were examined using linear mixed models for log10-transformed concentrations.

resultsIn 1,327 participants (60% Black participants and 60% women, the concentration of t-tau increased annually by 4.8% (95% CI = 4.0-5.6) and Nf-L by 5.9% (95% CI = 5.4-6.4). The longitudinal change in GFAP was higher among Black participants than among White participants (4.4% vs 3.5% per year, DISCUSSION: Blood biomarkers showed significant longitudinal changes corresponding to cognitive decline, clinical AD, and structural MRI characteristics. Our findings show that longitudinal changes in serum biomarkers were associated with several cognitive endophenotypes. CLASSIFICATION OF EVIDENCE: The study found Class II evidence that longitudinal changes in serum t-tau, Nf-L, and GFAP were associated with cognitive decline and the development of clinical AD in people older than 65 years.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesBiomarkersCognitionFemaleHumansMagnetic Resonance ImagingMaletau ProteinsAmyloid beta-PeptidesBiomarkerstau Proteins

Identifiers

PMID36446595
PMCPMC9984218
OpenAlexW4310465422

What OpenQuestion holds

Textmetadata
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.