Evidence map›Paper›PMID 27039903›Full record

ReviewCurrent neurology and neuroscience reports2016

New Genetic Approaches to AD: Lessons from APOE-TOMM40 Phylogenetics.

Michael W Lutz, Donna Crenshaw, Kathleen A Welsh-Bohmer, Daniel K Burns, Allen D Roses

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current neurology and neuroscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Frontiers in aging neuroscience · 2022
    Article
  10. Article
  11. Alzheimer's disease: a tale of two diseases?Neural regeneration research · 2021
    Review
  12. Article
  13. Article
  14. The ApoE Locus and COVID-19: Are We Going Where We Have Been?The journals of gerontology. Series A, Biological sciences and medical sciences · 2021
    Article
  15. MAPT haplotype-stratified GWAS reveals differential association for AD risk variants.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Article
  16. Haplotype architecture of the Alzheimer's risk in theAlzheimer's & dementia (Amsterdam, Netherlands) · 2020
    Article
  17. Article
  18. THE EXPOSOME IN HUMAN EVOLUTION: FROM DUST TO DIESEL.The Quarterly review of biology · 2019
    Article
  19. Review
  20. The Role of Irisin in Alzheimer's Disease.Journal of clinical medicine · 2018
    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

5 authors at 2 institutions in 1 country.

Michael W LutzJoseph and Kathleen Bryan Alzheimer's Disease Center, Department of Neurology, Duke University Medical Center, 2200 W Main Street, Suite A200, Durham, NC, 27705, USA.
Donna CrenshawZinfandel Pharmaceuticals, Inc., Durham, NC, USA.
Kathleen A Welsh-BohmerJoseph and Kathleen Bryan Alzheimer's Disease Center, Department of Neurology, Duke University Medical Center, 2200 W Main Street, Suite A200, Durham, NC, 27705, USA. kwe@duke.edu.
Daniel K BurnsZinfandel Pharmaceuticals, Inc., Durham, NC, USA.
Allen D RosesJoseph and Kathleen Bryan Alzheimer's Disease Center, Department of Neurology, Duke University Medical Center, 2200 W Main Street, Suite A200, Durham, NC, 27705, USA.
Duke Medical Center · USDuke University Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical trials for Alzheimer's disease are now focusing on the earliest stages of the disease with the goal of delaying dementia onset. There is great utility in using genetic variants to identify individuals at high age-dependent risk when the goal is to begin treatment before the development of any cognitive symptoms. Genetic variants identified through large-scale genome-wide association studies have not substantially improved the accuracy provided by APOE genotype to identify people at high risk of late-onset Alzheimer's disease (LOAD). We describe novel approaches, focused on molecular phylogenetics, to finding genetic variants that predict age at LOAD onset with sufficient accuracy and precision to be useful. We highlight the discovery of a polymorphism in TOMM40 that, in addition to APOE, may improve risk prediction and review how TOMM40 genetic variants may impact the develop of LOAD independently from APOE. The analysis methods described in this review may be useful for other genetically complex human diseases.

Indexed as

PhylogenyAlzheimer DiseaseAnimalsApolipoproteins EGenetic Predisposition to DiseaseHaplotypesHumansMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsRisk FactorsApolipoproteins EMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsTOMM40 protein, humanAlzheimer’s diseaseAPOEGenetic analysisPhylogenetic analysisRandomized clinical trialTOMM40

Identifiers

PMID27039903
OpenAlexW2337833545

What OpenQuestion holds

Textmetadata
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.