Evidence map›Paper›PMID 22832349›Full record

ArticleTranslational psychiatry2011

Metabolome in progression to Alzheimer's disease.

M Orešič, T Hyötyläinen, S-K Herukka, M Sysi-Aho, I Mattila, T Seppänan-Laakso, V Julkunen, P V Gopalacharyulu, M Hallikainen, J Koikkalainen and 4 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Translational psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 4 pooled it
8.1field-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

139 citing papers in PubMed, 4 syntheses or guidelines pooled it, 282 citations in OpenAlex.

  1. Pooled it
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  12. Metabolites and MRI-derived markers of dementia risk in a Puerto Rican cohort.Metabolomics : Official journal of the Metabolomic Society · 2025
    Article
  13. Metabolomics and lipidomics study on serum metabolite signatures in Alzheimer's disease and mild cognitive impairment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  14. Review
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79 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

14 authors at 4 institutions in 2 countries.

M OrešičVTT Technical Research Centre of Finland, Espoo, Finland. matej.oresic@vtt.fi
T Hyötyläinen
S-K Herukka
M Sysi-Aho
I Mattila
T Seppänan-Laakso
V Julkunen
P V Gopalacharyulu
M Hallikainen
J Koikkalainen
M Kivipelto
S Helisalmi
J Lötjönen
H Soininen
VTT Technical Research Centre of Finland · FIUniversity of Eastern Finland · FIKarolinska Institutet · SEKuopio University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mild cognitive impairment (MCI) is considered as a transition phase between normal aging and Alzheimer's disease (AD). MCI confers an increased risk of developing AD, although the state is heterogeneous with several possible outcomes, including even improvement back to normal cognition. We sought to determine the serum metabolomic profiles associated with progression to and diagnosis of AD in a prospective study. At the baseline assessment, the subjects enrolled in the study were classified into three diagnostic groups: healthy controls (n=46), MCI (n=143) and AD (n=47). Among the MCI subjects, 52 progressed to AD in the follow-up. Comprehensive metabolomics approach was applied to analyze baseline serum samples and to associate the metabolite profiles with the diagnosis at baseline and in the follow-up. At baseline, AD patients were characterized by diminished ether phospholipids, phosphatidylcholines, sphingomyelins and sterols. A molecular signature comprising three metabolites was identified, which was predictive of progression to AD in the follow-up. The major contributor to the predictive model was 2,4-dihydroxybutanoic acid, which was upregulated in AD progressors (P=0.0048), indicating potential involvement of hypoxia in the early AD pathogenesis. This was supported by the pathway analysis of metabolomics data, which identified upregulation of pentose phosphate pathway in patients who later progressed to AD. Together, our findings primarily implicate hypoxia, oxidative stress, as well as membrane lipid remodeling in progression to AD. Establishment of pathogenic relevance of predictive biomarkers such as ours may not only facilitate early diagnosis, but may also help identify new therapeutic avenues.

Indexed as

Disease ProgressionAgedAlzheimer DiseaseBiomarkersCognitive DysfunctionFemaleFollow-Up StudiesHumansMaleMetabolomePentose Phosphate PathwayPredictive Value of TestsBiomarkers

Identifiers

PMID22832349
PMCPMC3309497
OpenAlexW1981686145

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.