Evidence map›Paper›PMID 32439597›Full record

ReviewNeurobiology of disease2020

Genetic architecture of common non-Alzheimer's disease dementias.

Rita Guerreiro, Elizabeth Gibbons, Miguel Tábuas-Pereira, Celia Kun-Rodrigues, Gustavo C Santo, Jose Bras

Abstract readReview
In one paragraph

Review in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. A genome-wide association meta-analysis of all-cause and vascular dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Atrial Fibrillation and Other Cardiovascular Factors and the Risk of Dementia: An Italian Case-Control Study.International journal of environmental research and public health · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Heterozygous and Homozygous Variants inInternational journal of molecular sciences · 2022
    Article
  16. Article
  17. Review
  18. Article
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  20. Review
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

6 authors.

Rita GuerreiroCenter for Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, USA; Division of Psychiatry and Behavioral Medicine, Michigan State University College of Human Medicine, Grand Rapids, MI, USA. Electronic address: Rita.Guerreiro@vai.org.
Elizabeth GibbonsCenter for Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, USA.
Miguel Tábuas-PereiraDepartment of Neurology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal; Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Celia Kun-RodriguesCenter for Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, USA.
Gustavo C SantoDepartment of Neurology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal; Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Jose BrasCenter for Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, USA; Division of Psychiatry and Behavioral Medicine, Michigan State University College of Human Medicine, Grand Rapids, MI, USA.

Funding

Alzheimer's disease genetic architecture in the Portuguese populationR01AG067426 · NIA · VAN ANDEL RESEARCH INSTITUTE · PI GUERREIRO, RITA · 2020 to 2023
$3.1M
NIA NIH HHS R01 AG067426
6 · The paper itself

Abstract

Frontotemporal dementia (FTD), dementia with Lewy bodies (DLB) and vascular dementia (VaD) are the most common forms of dementia after Alzheimer's disease (AD). The heterogeneity of these disorders and/or the clinical overlap with other diseases hinder the study of their genetic components. Even though Mendelian dementias are rare, the study of these forms of disease can have a significant impact in the lives of patients and families and have successfully brought to the fore many of the genes currently known to be involved in FTD and VaD, starting to give us a glimpse of the molecular mechanisms underlying these phenotypes. More recently, genome-wide association studies have also pointed to disease risk-associated loci. This has been particularly important for DLB where familial forms of disease are very rarely described. In this review we systematically describe the Mendelian and risk genes involved in these non-AD dementias in an effort to contribute to a better understanding of their genetic architecture, find differences and commonalities between different dementia phenotypes, and uncover areas that would benefit from more intense research endeavors.

Indexed as

Frontotemporal DementiaGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLewy Body Disease

Identifiers

PMID32439597
PMCPMC8207829

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.