Evidence map›Paper›PMID 41949144›Full record

ArticleThe Indian journal of medical research2026

Blood level of β-amyloid, Tau, and p-Tau in mild cognitive impairment and Alzheimer disease: A follow up study.

Rashmita Pradhan, Sakshi Kumari, Abhinay Kumar Singh, Abhijith R Rao, Yudhishthir Yadav, Ashish Datt Upadhyay, Pramod Kumar Mehta, Aparajit B Dey, Sharmistha Dey

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Article in The Indian journal of medical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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9 authors.

Rashmita PradhanDepartment of Biophysics, All India Institute of Medical Sciences, New Delhi, India.
Sakshi KumariDepartment of Biophysics, All India Institute of Medical Sciences, New Delhi, India.
Abhinay Kumar SinghDepartment of Biophysics, All India Institute of Medical Sciences, New Delhi, India.
Abhijith R RaoDepartment of Geriatric Medicine, All India Institute of Medical Sciences, New Delhi, India.
Yudhishthir YadavDepartment of Biophysics, All India Institute of Medical Sciences, New Delhi, India.
Ashish Datt UpadhyayDepartment of Clinical Research Unit, All India Institute of Medical Sciences, New Delhi, India.
Pramod Kumar MehtaDepartment of Geriatric Medicine, All India Institute of Medical Sciences, New Delhi, India.
Aparajit B DeyDepartment of Geriatric Medicine, All India Institute of Medical Sciences, New Delhi, India.
Sharmistha DeyDepartment of Biophysics, All India Institute of Medical Sciences, New Delhi, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and objectives Deposition of β-amyloid and phosphorylated-tau proteins are major neuropathological abnormality in brain of patients with Alzheimer disease. This study aimed to study the role of various serum protein biomarkers to aid in the diagnosis and progression of Alzheimer disease. Methods Blood samples were collected from 96 patients with Alzheimer disease, 75 patients with mild cognitive impairment, and 70 geriatric controls at baseline. The number of patients (Alzheimer disease and mild cognitive impairment) who progressed after 1 year was 12, while the number of non-progressors was 24. Serum levels of β-amyloid1-42 (Aβ1-42), Tau, and phosphorylated-Tau181 (pTau) were quantified using surface plasmon resonance and further validated by Western blot. Results Comparison of proteins between the three groups revealed significantly lower Aβ1-42, higher Tau and pTau protein expression in serum of patients with Alzheimer disease as compared to patients with mild cognitive impairment and controls. In patients who progressed after one year, the baseline concentration of Aβ1-42 protein was significantly higher than their follow-up levels. Tau and pTau levels also increased significantly over the years. In non-progressors, no significant difference was observed in Aβ1-42, Tau, and pTau concentration between the baseline and follow up. Interpretation and conclusions Aβ1-42, Tau, and pTau proteins can serve as potential blood-based biomarkers for the diagnosis and monitoring the progression of Alzheimer disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCognitive Dysfunctiontau ProteinsAgedBiomarkersBrainDisease ProgressionFemaleFollow-Up StudiesHumansMaleMiddle AgedPeptide FragmentsPhosphorylationAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersMAPT protein, humanPeptide Fragmentstau ProteinsAlzheimer diseaseBiomarkerMild cognitive impairmentNon- progressorProgressorSurface plasmon resonance

Identifiers

PMID41949144
PMCPMC13104755

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