Evidence map›Paper›PMID 23816564›Full record

ReviewBiochimica et biophysica acta2014

Recent advances in the application of metabolomics to Alzheimer's Disease.

Eugenia Trushina, Michelle M Mielke

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 2 pooled it
8.3field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 2 syntheses or guidelines pooled it, 192 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Atractylenolide I mitigates Alzheimer's disease pathology in ApoEActa biochimica et biophysica Sinica · 2026
    Article
  8. Review
  9. Risk of Alzheimer's disease in Down syndrome: Insights gained by multi-omics.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  10. Article
  11. Article
  12. Journal of Alzheimer's disease reports · 2024
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Eugenia TrushinaDepartment of Neurology, Mayo Clinic, Rochester, MN 55905, USA; Department of Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: Trushina.Eugenia@mayo.edu.
Michelle M MielkeDepartment of Health Sciences Research, Division of Epidemiology, Mayo Clinic, Rochester, MN 55905, USA.
Mayo Clinic · USMayo Clinic in Florida · US

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
Longitudinal Study of Lipids and APOE in the Development of AD and AD PathologyU01AG037526 · NIA · MAYO CLINIC ROCHESTER · PI MIELKE, MICHELLE M · 2010 to 2014
$2.3M
Mitochondrial dynamics and metabolomic biomarkers in neurodegenerative disordersR01ES020715 · NIEHS · MAYO CLINIC ROCHESTER · PI TRUSHINA, EUGENIA · 2011 to 2015
$1.8M
NCATS NIH HHS UL1 TR000135NIA NIH HHS U01 AG037526NIEHS NIH HHS R01 ES020715NIEHS NIH HHS R01ES020715
6 · The paper itself

Abstract

The pathophysiological changes associated with Alzheimer's Disease (AD) begin decades before the emergence of clinical symptoms. Understanding the early mechanisms associated with AD pathology is, therefore, especially important for identifying disease-modifying therapeutic targets. While the majority of AD clinical trials to date have focused on anti-amyloid-beta (Aβ) treatments, other therapeutic approaches may be necessary. The ability to monitor changes in cellular networks that include both Aβ and non-Aβ pathways is essential to advance our understanding of the etiopathogenesis of AD and subsequent development of cognitive symptoms and dementia. Metabolomics is a powerful tool that detects perturbations in the metabolome, a pool of metabolites that reflects changes downstream of genomic, transcriptomic and proteomic fluctuations, and represents an accurate biochemical profile of the organism in health and disease. The application of metabolomics could help to identify biomarkers for early AD diagnosis, to discover novel therapeutic targets, and to monitor therapeutic response and disease progression. Moreover, given the considerable parallel between mouse and human metabolism, the use of metabolomics provides ready translation of animal research into human studies for accelerated drug design. In this review, we will summarize current progress in the application of metabolomics in both animal models and in humans to further understanding of the mechanisms involved in AD pathogenesis.

Indexed as

Alzheimer DiseaseAnimalsDisease Models, AnimalHumansMetabolomicsAlzheimer's DiseaseAnimal modelsBiomarkersCerebrospinal fluidMetabolomicsPlasma

Identifiers

PMID23816564
PMCPMC3842412
OpenAlexW1994243437

What OpenQuestion holds

Textmetadata
LicenceTDM
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.