Evidence map›Paper›PMID 36810164›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2023

Levels of Soluble Interleukin 6 Receptor and Asp358Ala Are Associated With Cognitive Performance and Alzheimer Disease Biomarkers.

Daniel Quillen, Timothy M Hughes, Suzanne Craft, Timothy Howard, Thomas Register, Cynthia Suerken, Gregory A Hawkins, Carol Milligan

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

Article in Neurology(R) neuroimmunology & neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 20 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.

Daniel QuillenFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine.
Timothy M HughesFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine.
Suzanne CraftFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine.
Timothy HowardFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine.
Thomas RegisterFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine.
Cynthia SuerkenFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine.
Gregory A HawkinsFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine.
Carol MilliganFrom the The Neuroscience Program (D.Q., T.M.H., G.A.H., C.M.); Department of Neurobiology and Anatomy (D.Q., C.M.); Department of Internal Medicine, Gerontology and Geriatric Medicine (T.M.H., S.C.); Alzheimer's Disease Research Center (T.M.H., S.C., T.R., C.M.); Department of Biochemistry (T.H., T.R., G.A.H.); and Department of Biostatics and Data Science (C.S.), Wake Forest School of Medicine. milligan@wakehealth.edu.
Alzheimer’s Disease Neuroimaging Initiative · US

Funding

Wake Forest University School of Medicine Alzheimer's Disease Research CenterP30AG072947 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SUZANNE CRAFT · 2021 to 2026
$24.3M
NIA NIH HHS P30 AG072947
6 · The paper itself

Abstract

BACKGROUND AND

objectivesAlzheimer disease (AD) is a neurodegenerative disease process manifesting clinically with cognitive impairment and dementia. AD pathology is complex, and in addition to plaques and tangles, neuroinflammation is a consistent feature. Interleukin (IL) 6 is a multifaceted cytokine involved in a plethora of cellular mechanisms including both anti-inflammatory and inflammatory processes. IL6 can signal classically through the membrane-bound receptor or by IL6 trans-signaling forming a complex with the soluble IL6 receptor (sIL6R) and activating membrane-bound glycoprotein 130 on cells not expressing IL6R. IL6 trans-signaling has been demonstrated as the primary mechanism of IL6-mediated events in neurodegenerative processes. In this study, we performed a cross-sectional analysis to investigate whether inheritance of a genetic variation in the

methodsWe genotyped the

resultsWe found that inheritance of the DISCUSSION: These data suggest that IL6 trans-signaling and the inheritance of the

Indexed as

Alzheimer DiseaseCognitionReceptors, Interleukin-6BiomarkersCross-Sectional StudiesHumansInterleukin-6Prospective StudiesBiomarkersInterleukin-6Receptors, Interleukin-6

Identifiers

PMID36810164
PMCPMC9944616
OpenAlexW4321434823

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.