Evidence map›Paper›PMID 37016464›Full record

ArticleAlzheimer's research & therapy2023

APOE ε4 gene dose effect on imaging and blood biomarkers of neuroinflammation and beta-amyloid in cognitively unimpaired elderly.

Anniina Snellman, Laura L Ekblad, Jouni Tuisku, Mikko Koivumäki, Nicholas J Ashton, Juan Lantero-Rodriguez, Thomas K Karikari, Semi Helin, Marco Bucci, Eliisa Löyttyniemi and 6 more

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Neuroinflammation demonstrated byAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. How to measure and model cardiovascular aging.Cardiovascular research · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. SV2A PET shows hippocampal synaptic loss in cognitively unimpaired APOE ε4/ε4 homozygotes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  14. Article
  15. APOE ε4 carrier status modifies plasma p-tau181 concentrations in cognitively healthy super-seniors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Insulin resistance and body mass index are associated with TSPO PET in cognitively unimpaired elderly.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    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

16 authors at 8 institutions in 5 countries.

Anniina SnellmanTurku PET Centre, University of Turku, Turku University Hospital, Kiinamyllynkatu 4-8, 20520, Turku, Finland. aepakk@utu.fi.
Laura L EkbladTurku PET Centre, University of Turku, Turku University Hospital, Kiinamyllynkatu 4-8, 20520, Turku, Finland.
Jouni TuiskuTurku PET Centre, University of Turku, Turku University Hospital, Kiinamyllynkatu 4-8, 20520, Turku, Finland.
Mikko KoivumäkiTurku PET Centre, University of Turku, Turku University Hospital, Kiinamyllynkatu 4-8, 20520, Turku, Finland.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Juan Lantero-RodriguezDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Thomas K KarikariDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Semi HelinTurku PET Centre, University of Turku, Turku University Hospital, Kiinamyllynkatu 4-8, 20520, Turku, Finland.
Marco BucciTurku PET Centre, University of Turku, Turku University Hospital, Kiinamyllynkatu 4-8, 20520, Turku, Finland.
Eliisa LöyttyniemiDepartment of Biostatistics, University of Turku, Turku, Finland.
Riitta ParkkolaDepartment of Radiology, Turku University Hospital, University of Turku, Turku, Finland.
Mira KarraschDepartment of Psychology, Åbo Akademi University, Turku, Finland.
Michael SchöllDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Juha O RinneTurku PET Centre, University of Turku, Turku University Hospital, Kiinamyllynkatu 4-8, 20520, Turku, Finland.
University of Turku · FITurku University Hospital · FIUniversity of Gothenburg · SETurku PET Centre · FIÅbo Akademi University · FIStavanger University Hospital · NOUK Dementia Research Institute · GBUniversity College London · GB

Funding

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 AG068398
6 · The paper itself

Abstract

backgroundNeuroinflammation, characterized by increased reactivity of microglia and astrocytes in the brain, is known to be present at various stages of the Alzheimer's disease (AD) continuum. However, its presence and relationship with amyloid pathology in cognitively normal at-risk individuals is less clear. Here, we used positron emission tomography (PET) and blood biomarker measurements to examine differences in neuroinflammation and beta-amyloid (Aβ) and their association in cognitively unimpaired homozygotes, heterozygotes, or non-carriers of the APOE ε4 allele, the strongest genetic risk for sporadic AD.

methodsSixty 60-75-year-old APOE ε4 homozygotes (n = 19), heterozygotes (n = 21), and non-carriers (n = 20) were recruited in collaboration with the local Auria biobank. The participants underwent

resultsIn our cognitively unimpaired sample, cortical

conclusionsOnly Aβ burden measured by PET, but not markers of neuroinflammation, differed among cognitively unimpaired elderly with different APOE ε4 gene dose. However, APOE ε4 gene dose seemed to modulate the association between neuroinflammation and Aβ.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4Gene DosageAgedApolipoproteins EBiomarkersGenotypeHumansNeuroinflammatory DiseasesPositron-Emission TomographyReceptors, GABAAmyloid beta-PeptidesApoE protein, humanApolipoprotein E4Apolipoproteins EBiomarkersReceptors, GABATSPO protein, humanAlzheimer’s diseaseAPOEApolipoprotein EAstrocytesBeta-amyloidBiomarkerGFAPMicrogliaPETTSPO

Identifiers

PMID37016464
PMCPMC10071691
OpenAlexW4362555151

What OpenQuestion holds

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LicenceCC BY
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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.