Evidence mapPaperPMID 42250049Full record

ReviewMetabolic brain disease2026

Omics-driven strategies for identifying biomarkers in Alzheimer's disease.

Yumna Khan, Arcot Rekha, Suhas Ballal, Laxmidhar Maharana, Mudasir Maqbool, Kavita Goyal, Rakhi Mishra, Prerna Uniyal, Prawez Alam, Tariq Mohammed Aljarba and 2 more

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In one paragraph

Review in Metabolic brain disease, 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

12 authors.

Yumna KhanIndependent Researcher, Abu Dhabi, United Arab Emirates.
Arcot RekhaDr. D.Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth University, Pimpri, Pune, Maharashtra, India.
Suhas BallalDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India.
Laxmidhar MaharanaDepartment of General Medicine, IMS & SUM Hospital, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha, 751030, India.
Mudasir MaqboolDepartment of Pharmacology, Government Medical College Baramulla, Jammu, Kashmir, 193103, India.
Kavita GoyalSharda University, Greater Noida, Uttar Pradesh, India.
Rakhi MishraNoida Institute of Engineering and Technology (Pharmacy Institute), 19 Knowledge Park 2 , Greater Noida, India.
Prerna UniyalFaculty of Pharmacy, Graphic Era Hill University, Clement Town, Dehradun, Uttarakhand, 248002, India.
Prawez AlamDepartment of Pharmacognosy, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, 11942, Saudi Arabia.
Tariq Mohammed AljarbaDepartment of Pharmacognosy, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj, 11942, Saudi Arabia.
Gaurav GuptaCentre for Research Impact & Outcome-Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India.
Md Sadique HussainUttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Prem Nagar, Dehradun, Uttarakhand, 248007, India. sadiquehussain@uumail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with limited treatment options, mainly due to late diagnosis and partial understanding of its molecular aspects. Traditional biomarker discovery approaches have significantly contributed to AD diagnostics but suffer from limitations. The advent of omics technologies (genomics, epigenomics, transcriptomics, proteomics, and metabolomics) has revolutionized the search for novel biomarkers by enabling comprehensive molecular profiling. Genomic studies have identified risk-associated variants such as APOE4, while epigenomic alterations, including DNA methylation alterations, offer insight into gene regulation in AD. Transcriptomic analyses, particularly single-cell and spatial transcriptomics, have uncovered molecular pathways linked to neuroinflammation and synaptic dysfunction. Proteomic advancements, including mass spectrometry and extracellular vesicle profiling, have identified potential blood- and CSF-based biomarkers for early-stage detection. Metabolomic and lipidomic studies indicate that cerebral glucose hypometabolism, insulin resistance, mitochondrial damage, redox imbalance, and disrupted lipid homeostasis are centra contributors to AD pathogenesis rather than secondary considerations of the disease. These metabolic dysfunctions may precede overt neurodegeneration and influence amyloid processing, tau phosphorylation, neuroinflammatory activation, and synaptic loss, thereby generating clinically informative biomarker signatures in blood and cerebrospinal fluid. Within this metabolism-centered paradigm, integrative multi-omics approaches are particularly valuable because they not only enhance biomarker specificity, but also connect molecular signatures with bioenergetic and immune-mediated mechanisms of disease. Accordingly, integrative multi-omics approaches improve biomarker specificity and predictive power, thereby supporting the development of precision medicine and targeted therapeutic interventions. Nevertheless, important challenges remain, including data integration, reproducibility, and clinical translation.

Indexed as

Alzheimer DiseaseBiomarkersGenomicsMetabolomicsProteomicsAnimalsEpigenomicsHumansMultiomicsBiomarkersBiomarkersEarly diagnosisMulti-Omics approachesTranslational research

Identifiers

PMID42250049

What Socratic holds

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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.