Evidence map›Paper›PMID 28825204›Full record

ReviewCurrent neurology and neuroscience reports2017

Genetics of Alzheimer's Disease: the Importance of Polygenic and Epistatic Components.

Neha Raghavan, Giuseppe Tosto

Abstract readReview
In one paragraph

Review in Current neurology and neuroscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Shorter Telomere Length in Individuals with Neurocognitive Disorder andInternational journal of molecular sciences · 2025
    Article
  6. Genetic diversity promotes resilience in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Genetics of Alzheimer's disease.Wiener medizinische Wochenschrift (1946) · 2021
    Review
  18. Article
  19. Article
  20. Early detection and personalized medicine: Future strategies against Alzheimer's disease.Progress in molecular biology and translational science · 2021
    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

2 authors.

Neha RaghavanThe Gertrude H. Sergievsky Center, College of Physicians and Surgeons, Columbia University, 622 W. 168th Street PH 19-314, New York, NY, 10032, USA.
Giuseppe TostoThe Gertrude H. Sergievsky Center, College of Physicians and Surgeons, Columbia University, 622 W. 168th Street PH 19-314, New York, NY, 10032, USA. gt2260@cumc.columbia.edu.

Funding

Admixture mapping in late-onset Alzheimer’s diseaseR21AG054832 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TOSTO, GIUSEPPE · 2016 to 2017
$440k
NIA NIH HHS R21 AG054832
6 · The paper itself

Abstract

purpose of reviewWe aimed to summarize the recent advances in genetic findings of Alzheimer's disease (AD), focusing on traditional single-marker and gene approaches and non-traditional ones, i.e., polygenic and epistatic components. RECENT

findingsGenetic studies have progressed over the last few decades from linkage to genome-wide association studies (GWAS), and most recently studies utilizing high-throughput sequencing. So far, GWASs have identified several common variants characterized by small effect sizes (besides APOE-ε4). Sequencing has facilitated the study of rare variants with larger effects. Nevertheless, missing heritability for AD remains extensive; a possible explanation might lie in the existence of polygenic and epistatic components. We review findings achieved by single-marker approaches, but also polygenic and epistatic associations. The latter two are critical, yet-underexplored mechanisms. Genes involved in complex diseases are likely regulated by mechanisms and pathways involving many other genes, an aspect potentially missed by traditional approaches.

Indexed as

Alzheimer DiseaseEpistasis, GeneticGenetic MarkersGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPolymorphism, Single NucleotideGenetic MarkersEpistasisGWASNext-generation sequencingPolygenic risk score

Identifiers

PMID28825204
PMCPMC5699909

What OpenQuestion holds

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Registered trials

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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.