Evidence map›Paper›PMID 39012677›Full record

ArticleAging and disease2024

Dysregulation of Lipid Metabolism Serves as A Link Between Alzheimer's and Cardiovascular Disease, As Witnessed in A Cross-Sectional Study.

Laura Mourino-Alvarez, Cristina Juarez-Alia, Tamara Sastre-Oliva, Inés Perales-Sánchez, German Hernandez-Fernandez, Eduardo Chicano-Galvez, Ángela Peralbo-Molina, Felipe Madruga, Emilio Blanco-Lopez, Teresa Tejerina and 1 more

Abstract read
In one paragraph

Article in Aging and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Alterations in the inflammatory homeostasis of aging-related cardiac dysfunction and Alzheimer's diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  4. Article
  5. 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

11 authors.

Laura Mourino-AlvarezDepartment of Vascular Physiopathology, Hospital Nacional de Paraplejicos, SESCAM, 45071 Toledo, Spain.
Cristina Juarez-AliaDepartment of Vascular Physiopathology, Hospital Nacional de Paraplejicos, SESCAM, 45071 Toledo, Spain.
Tamara Sastre-OlivaDepartment of Vascular Physiopathology, Hospital Nacional de Paraplejicos, SESCAM, 45071 Toledo, Spain.
Inés Perales-SánchezDepartment of Vascular Physiopathology, Hospital Nacional de Paraplejicos, SESCAM, 45071 Toledo, Spain.
German Hernandez-FernandezDepartment of Vascular Physiopathology, Hospital Nacional de Paraplejicos, SESCAM, 45071 Toledo, Spain.
Eduardo Chicano-GalvezIMIBIC Mass Spectrometry and Molecular Imaging Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba (UCO), Córdoba, Spain.
Ángela Peralbo-MolinaIMIBIC Mass Spectrometry and Molecular Imaging Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba (UCO), Córdoba, Spain.
Felipe MadrugaDepartament of Geriatrics, Hospital Virgen del Valle, SESCAM, Toledo, Spain.
Emilio Blanco-LopezDepartment of Cardiology, Ciudad Real General University Hospital, Ciudad Real, Spain.
Teresa TejerinaDepartment of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
María G BarderasDepartment of Vascular Physiopathology, Hospital Nacional de Paraplejicos, SESCAM, 45071 Toledo, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular risk factors and established cardiovascular disease (CVD) increase the risk of suffering dementia of the Alzheimer's type (DAT). Here, we set out to define specific molecular profiles of CVD in patients with DAT to better understand its relationship, to unravel the mechanisms underlying the high risk of developing DAT in CVD patients and to define new markers of early disease. Plasma samples from patients with DAT, with and without CVD, were analyzed through a multiomics approach, with integration of metabolomics and proteomics datasets using the OmicsNet web-based tool. Metabolomics results showed an enrichment in lipids and lipid-like molecules. Similarly, the most significant cluster identified through proteomics was formed by 5 proteins related to lipoprotein and cholesterol metabolism. After integration and functional enrichment, glycerolipid metabolism, fatty acid degradation and sphingolipid metabolism were among the most significant functions. Finally, the differential expression of ABCA1 and APOH proteins was verified, in an independent cohort also including controls and patients with CVD alone. Both proteins positively correlated with phospho-Tau (181), a classical hallmark of DAT. Different molecular profiles exist in patients with DAT, with and without CVD, with exacerbated alterations in patients in which DAT and CVD co-exist. This information may help to define biomarkers like ABCA1 and APOH that identify patients with cardiovascular dysfunction that are at high risk of developing DAT. Such markers will allow more personalized interventions to be selected, a further step towards precision medicine for individuals whose molecular profiles indicate a distinct response to the same management strategies.

Indexed as

Alzheimer DiseaseCardiovascular DiseasesLipid MetabolismAgedAged, 80 and overATP Binding Cassette Transporter 1BiomarkersCross-Sectional StudiesFemaleHumansMaleMetabolomicsMiddle AgedProteomicsABCA1 protein, humanATP Binding Cassette Transporter 1Biomarkers

Identifiers

PMID39012677
PMCPMC12096944

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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.