ArticleBrain communications2025
Comprehensive metabolomics profiling reveals novel biomarkers and pathways for early detection of Alzheimer's disease.
Article in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Omics-driven strategies for identifying biomarkers in Alzheimer's disease.Metabolic brain disease · 2026Review
- Efficacy ofJMIR research protocols · 2026Article
- Serum metabolomic profiling following cerebellar repetitive transcranial magnetic stimulation combined with cognitive training on Alzheimer's disease.Frontiers in neurology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is a multifactorial neurodegenerative disorder marked by cognitive decline, synaptic dysfunction, and metabolic alterations. This study investigated disease-associated profiles in the Indian population using integrated clinical, metabolomic, and plasma biomarker analyses. We enrolled 25 clinically diagnosed patients (mean age: 61.20 ± 7.76 years) and 25 cognitively healthy controls (mean age: 60.56 ± 7.48 years). Cognitive and neuropsychiatric assessments included Addenbrooke's Cognitive Examination-III, Clinical Dementia Rating-Global, and Patient Health Questionnaire-9 for patients, and Montreal Cognitive Assessment, Clinical Dementia Rating-Global, and Patient Health Questionnaire-9 for controls. Plasma metabolomics was performed using liquid chromatography-mass spectrometry, and targeted ELISA quantified amyloid beta 40, amyloid beta 42, phosphorylated tau181, phosphorylated tau217, neurofilament light chain, apolipoprotein E, APOE4, 8-hydroxy-2'-deoxyguanosine, C-reactive protein, brain-derived neurotrophic factor, and glutamate. Statistical analyses included principal component analysis, volcano plots, receiver operating characteristic curves, pathway enrichment, and correlation analyses. Patients showed reduced cognition (median Addenbrooke's Cognitive Examination-III: 26). Clinical Dementia Rating-Global scores (1.44 ± 0.65 versus 0.24 ± 0.25;
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.