Evidence map›Paper›PMID 31915256›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

Longitudinal Basal Forebrain Degeneration Interacts with TREM2/C3 Biomarkers of Inflammation in Presymptomatic Alzheimer's Disease.

Taylor W Schmitz, Hermona Soreq, Judes Poirier, R Nathan Spreng

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. A lifespan staging model of basal forebrain cholinergic vulnerability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  2. The neuromodulatory fragility hypothesis of Alzheimer's disease pathogenesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Sex-dependent cholinergic effects on amyloid pathology: A translational study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Observational
  16. Article
  17. Review
  18. Microglia Biomarkers in Alzheimer's Disease.Molecular neurobiology · 2021
    Review
  19. Article
  20. Article
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

4 authors at 3 institutions in 2 countries.

Taylor W SchmitzDepartment of Physiology and Pharmacology, University of Western Ontario, London, Ontario N6A5C1, Canada, taylor.schmitz@gmail.com.ORCID 0000-0003-0585-7524
Hermona SoreqEdmond & Lily Safra Center for Brain Sciences and the Department of Biological Chemistry, Hebrew University of Jerusalem, Jerusalem, 9190401 Israel.
Judes PoirierCentre for Studies in the Prevention of Alzheimer's Disease, Douglas Mental Health University Institute, Verdun, Quebec, HRH 1R3 Canada.ORCID 0000-0002-8018-4545
R Nathan SprengCentre for Studies in the Prevention of Alzheimer's Disease, Douglas Mental Health University Institute, Verdun, Quebec, HRH 1R3 Canada.ORCID 0000-0003-1530-8916
Montreal Neurological Institute and Hospital · CAHebrew University of Jerusalem · ILWestern University · CA

Funding

In vivo staging of preclinical Alzheimer's disease progressionR03AG060263 · NIA · MCGILL UNIVERSITY · PI SPRENG, ROBERT NATHAN · 2018 to 2019
$106k
NIA NIH HHS R03 AG060263
6 · The paper itself

Abstract

Cholinergic inputs originating from the peripheral nervous system regulate the inflammatory immune responses of macrophages during clearance of blood-based pathogens. Because microglia are involved in clearing amyloid and tau pathology from the central nervous system, we hypothesized that cholinergic input originating from the basal forebrain might similarly regulate inflammatory immune responses to these pathologies in the aging brain. To explore this hypothesis, we leveraged the Alzheimer's Disease Neuroimaging Initiative dataset. Cognitively normal older male and female human adults were differentiated according to the relative concentration of phosphorylated tau and amyloid in their cerebrospinal fluid, yielding neurotypical and preclinical, cognitively healthy, subgroups. We then tracked these two groups longitudinally with structural MRI and biomarkers of inflammation, including soluble sTREM2 levels in the CSF and complement

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloidApolipoproteins EBasal ForebrainBiomarkersComplement C3EncephalitisFemaleGray MatterHumansLongitudinal StudiesMagnetic Resonance ImagingMaleMembrane GlycoproteinsAmyloidApolipoproteins EBiomarkersC3 protein, humanComplement C3Membrane GlycoproteinsReceptors, Immunologictau ProteinsTREM2 protein, humanamyloidbasal forebrain cholinergic systemcomplement C3phosphorylated taupreclinical Alzheimer's diseasesoluble TREM2

Identifiers

PMID31915256
PMCPMC7046458
OpenAlexW2999746599

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.