Evidence mapPaperPMID 41924010Full record

ArticleFrontiers in neuroscience2026

Untargeted plasma metabolomics in canine cognitive dysfunction: the naturally occurring Alzheimer's disease analog in dogs.

Tonatiuh Melgarejo, Scarlett Harrison, Yan Chang, Miriam Munoz, Maya Kim, Youna Choi, Joyce G Riveroll-Gonzalez, Barbara Natterson-Horowitz, Annika Linde

Abstract read
In one paragraph

Article in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Tonatiuh MelgarejoCollege of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, United States.
Scarlett HarrisonModern Animal Hospital, Los Angeles, CA, United States.
Yan ChangCollege of Veterinary Medicine & Biomedical Sciences, Colorado State University, Fort Collins, CO, United States.
Miriam MunozCollege of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, United States.
Maya KimSchool of Veterinary Medicine, Ross University, Basseterre, Saint Kitts and Nevis.
Youna ChoiCollege of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, United States.
Joyce G Riveroll-GonzalezCollege of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, United States.
Barbara Natterson-HorowitzDepartment of Global Health and Social Medicine, Harvard Medical School, Boston, MA, United States.
Annika LindeCollege of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Canine Cognitive Dysfunction (CCD) is an increasingly prevalent naturally occurring neurodegenerative condition in senescent dogs that share neuropathological and clinical features with human Alzheimer's disease (AD). Metabolic profiling allows for identification of new candidates for AD biomarkers, diagnostics, and therapeutics. Despite its translational potential, plasma metabolomic profiling of dogs with CDD has not been previously characterized. Methods: This case-control study analyzed plasma samples from ten client-owned geriatric dogs, including five with severe CCD and five age-matched, clinically healthy controls. Untargeted plasma metabolomics was performed using ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). Multivariate and univariate statistical analyses identified significant metabolic differences between the groups. Metabolites were considered significant based on a variable importance in projection (VIP) score > 1.5, fold change (FC) > 2.0, and adjusted Results: Fifteen metabolites across seven chemical classes were significantly altered in CCD dogs compared to controls, including glycerophospholipids, steroid derivatives, indoles, and mitochondrial-related compounds. Notably, elevated lysophosphatidic acid (LPA 20:2/0:0) and reduced ubiquinone-2 levels suggest dysregulation in neuroinflammatory and oxidative stress pathways. Cholesterol exhibited the highest FC and VIP scores, further reinforcing its role in AD pathogenesis. Hierarchical clustering and pathway enrichment analyses supported distinct metabolic signatures in CCD that mirror those observed in human AD. Discussion: This is the first untargeted plasma metabolomic profiling of dogs with CCD, revealing systemic metabolic disturbances that align with AD pathophysiology. Data was collected from senescent community-dwelling companion dogs, which enhances the study's ecological and translational relevance. It supports the utility of CCD as an AD model and highlight candidate plasma biomarkers that warrant further investigation. Future longitudinal studies integrating metabolomics with neuroimaging, histopathology, and behavioral assessments are required to validate these findings and contribute to AD biomarker discovery and therapeutic development.

Indexed as

agingbiomarkerscanine dementiacompanion dogscomparative neuropathologylipid metabolismtranslational modeluntargeted metabolomics

Identifiers

PMID41924010
PMCPMC13036105

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.