Evidence map›Paper›PMID 34615922›Full record

ArticleScientific reports2021

Genetic effects on longitudinal cognitive decline during the early stages of Alzheimer's disease.

Atul Kumar, Maryam Shoai, Sebastian Palmqvist, Erik Stomrud, John Hardy, Niklas Mattsson-Carlgren, Oskar Hansson

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

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Protective Effects of Genetic Proxies of Cognitive Reserve in Parkinson's Disease: A Longitudinal Multi-Cohort Study.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Cognitive trajectories diverge by genetic risk in a preclinical longitudinal cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  10. Article
  11. Article
  12. 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

7 authors at 3 institutions in 4 countries.

Atul KumarClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden. atul.kumar@med.lu.se.
Maryam ShoaiUK Dementia Research Institute and Department of Neurodegenerative Disease and Reta Lila Weston Institute, UCL Queen Square Institute of Neurology and UCL Movement Disorders Centre, University College London, London, WC1V 6LJ, UK.
Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Erik StomrudClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
John HardyUK Dementia Research Institute and Department of Neurodegenerative Disease and Reta Lila Weston Institute, UCL Queen Square Institute of Neurology and UCL Movement Disorders Centre, University College London, London, WC1V 6LJ, UK.
Niklas Mattsson-CarlgrenClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Lund University · SEHong Kong University of Science and Technology · HKUK Dementia Research Institute · GB

Funding

Medical Research Council G0701075Medical Research Council G0901254Medical Research Council G1001253Medical Research Council MR/J004758/1Medical Research Council MR/K01417X/1Medical Research Council MR/L501542/1Parkinson's UK G-0907Parkinson's UK G-1307
6 · The paper itself

Abstract

Cognitive decline in early-stage Alzheimer's disease (AD) may depend on genetic variability. In the Swedish BioFINDER study, we used polygenic scores (PGS) (for AD, intelligence, and educational attainment) to predict longitudinal cognitive change (measured by mini-mental state examination (MMSE) [primary outcome] and other cognitive tests) over a mean of 4.2 years. We included 260 β-amyloid (Aβ) negative cognitively unimpaired (CU) individuals, 121 Aβ-positive CU (preclinical AD), 50 Aβ-negative mild cognitive impairment (MCI) patients, and 127 Aβ-positive MCI patients (prodromal AD). Statistical significance was determined at Bonferroni corrected p value < 0.05. The PGS for intelligence (beta = 0.1, p = 2.9e-02) was protective against decline in MMSE in CU and MCI participants regardless of Aβ status. The polygenic risk score for AD (beta =  - 0.12, p = 9.4e-03) was correlated with the rate of change in MMSE and was partially mediated by Aβ-pathology (mediation effect 20%). There was no effect of education PGS on cognitive measures. Genetic variants associated with intelligence mitigate cognitive decline independent of Aβ-pathology, while effects of genetic variants associated with AD are partly mediated by Aβ-pathology.

Indexed as

Genetic Predisposition to DiseaseAgedAged, 80 and overAlgorithmsAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersCognitive DysfunctionComputational BiologyFemaleGene Expression ProfilingGenetic Association StudiesGenetic VariationGenotypeHumansMaleAmyloid beta-PeptidesBiomarkers

Identifiers

PMID34615922
PMCPMC8494841
OpenAlexW3130382842

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.