Evidence map›Paper›PMID 30776473›Full record

ArticleBrain, behavior, and immunity2019

Microglia - mediated immunity partly contributes to the genetic association between Alzheimer's disease and hippocampal volume.

T M Lancaster, M J Hill, R Sims, J Williams

Open access · hybridAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Early microglial priming in Alzheimer's disease revealed by ME-seq.bioRxiv : the preprint server for biology · 2026
    Article
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  10. Review
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  15. Microglia Biomarkers in Alzheimer's Disease.Molecular neurobiology · 2021
    Review
  16. Article
  17. Review
  18. Polygenic risk for Alzheimer's disease shapes hippocampal scene-selectivity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Article
  19. Review
  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 2 institutions in 1 country.

T M LancasterUK Dementia Research Institute, School of Medicine, Cardiff University, UK; Cardiff University Brain Research Imaging Centre (CUBRIC), School of Psychology, Cardiff University, UK; MRC Centre of Neuropsychiatric Genetics & Genomics, School of Medicine, Cardiff University, UK. Electronic address: LancasterTM@cardiff.ac.uk.
M J HillUK Dementia Research Institute, School of Medicine, Cardiff University, UK; MRC Centre of Neuropsychiatric Genetics & Genomics, School of Medicine, Cardiff University, UK.
R SimsUK Dementia Research Institute, School of Medicine, Cardiff University, UK; MRC Centre of Neuropsychiatric Genetics & Genomics, School of Medicine, Cardiff University, UK.
J WilliamsUK Dementia Research Institute, School of Medicine, Cardiff University, UK; MRC Centre of Neuropsychiatric Genetics & Genomics, School of Medicine, Cardiff University, UK.
Cardiff University · GBGenomics (United Kingdom) · GB

Funding

Medical Research Council G0300429Medical Research Council G0600237Medical Research Council G0800509Medical Research Council G0801418Medical Research Council G0902227Medical Research Council G9810900Medical Research Council MC_PC_17112Medical Research Council MR/K013041/1Medical Research Council MR/L010305/1Medical Research Council MR/L023784/1Medical Research Council MR/L023784/2Medical Research Council MR/L501517/1Medical Research Council MR/M009076/1Wellcome TrustWellcome Trust 513688
6 · The paper itself

Abstract

Genome-wide association studies (GWAS) suggest that Alzheimer's disease (AD) is partly explained by a burden of risk alleles (single nucleotide polymorphisms; SNPs) with relatively small effects. However, the mechanisms by which these loci cumulatively confer susceptibility remain largely unknown. Accumulating evidence suggests an association between increased AD risk allele burden (measured via a polygenic risk profile score; AD-RPS) with reduced hippocampal volume (HV) across a number of independent cohorts. These lines of research suggest that the reduced HV may be a causal mechanism of risk in the development of late-onset Alzheimer's disease (AD). However, as RPS assesses broad, cumulative genetic risk, little is known about the biological processes which may explain this observation. Here, we leverage GWAS data from i) 17,008 late onset AD cases & 37,154 controls and ii) hippocampal volume (N = 12,147; N = 9707) to explore putative pathways that may explain this association. We first demonstrate an association between whole genome AD-RPS and HV (PT < 0.5, Z = -2.07, P = 0.038), confirming previous associations. Second, we restrict our analysis to SNPs within AD genes within a microglia mediated immunity network (N

Indexed as

AllelesAlzheimer DiseaseCase-Control StudiesDatabases, GeneticFemaleGene FrequencyGenetic Predisposition to DiseaseGenome-Wide Association StudyHippocampusHumansMagnetic Resonance ImagingMaleMicrogliaMultifactorial InheritancePolymorphism, Single NucleotideRisk FactorsAlzhiemer’s diseaseGWASHippocampusMicrogliaMRIPolygenicRisk profile score

Identifiers

PMID30776473
PMCPMC6605284
OpenAlexW2914235110

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.