ArticleProteomics2026
Coupling CZE, Liquid-Phase Ion Mobility, to MS/MS for Quantitative Top-Down Proteomics: Revealing Significant Proteoform Differences Between Healthy and Alzheimer's Disease Brains.
Article in Proteomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- A Draft Map of E. coli Proteoforms.Analytical chemistry · 2026Article
- Advancing the Reproducibility and Repeatability of Capillary Zone Electrophoresis-Mass Spectrometry-Based Top-Down Proteomics by an Improved Capillary Coating Procedure.Journal of proteome research · 2026Article
- Top-Down Mass Spectrometry and Its Current Applications in Biomarker Discovery in Aging and Age-Related Diseases.International journal of molecular sciences · 2026Review
- Article
- Recent Developments and Applications of Capillary and Microchip Electrophoresis in Proteomics and Peptidomics (2023-2025).Journal of separation science · 2026Review
- Extensive Backbone Cleavage Coverage of Intact Proteoforms in a Mass Range of 10-70 kDa by Integrating Electron, Collision, and Photon-Based Fragmentation Techniques during an Electrophoretic Time Scale.Journal of the American Society for Mass Spectrometry · 2026Article
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4 authors.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline and pathological protein aggregation. Comprehensive quantitative proteomics of brain tissues from AD patients is critical for pursuing a better understanding of the molecular mechanisms that drive AD progression. Here, we present one of the first quantitative top-down proteomics (TDP) studies of postmortem cortex samples from AD patients and healthy controls to profile their proteoform differences by coupling capillary zone electrophoresis (CZE, liquid-phase ion mobility) to tandem mass spectrometry (MS/MS). We identified 3191 unique proteoforms and uncovered a drastic transformation in the proteoform profile in AD compared to healthy controls. Over 2200 proteoforms were exclusively identified in either AD or healthy control samples, and 157 proteoforms identified in both AD and control samples showed statistically significant abundance differences between the two conditions. Gene Ontology and pathway analysis of the genes associated with those proteoforms revealed broad changes in biological processes in AD brains, for example, telomere organization, substantia nigra development, amyloid fibril formation, microtubule cytoskeleton organization, progressive neurological disorders, long-term synaptic potentiation, and axogenesis. These biological processes are highly associated with the development of AD. Our study revealed a pool of potential novel proteoform biomarkers of AD in human brain samples for early diagnosis and therapy development. SUMMARY: Alzheimer's disease (AD) is a chronic neurodegenerative disease, destroying brain cells and causing thinking ability and memory to decline over time. Proteins (e.g., amyloid and tau) play key roles in the development of AD. Global and accurate protein measurement of human brains of AD patients and healthy controls will shed new light on the molecular mechanisms driving AD progression and discover new biomarkers for AD diagnosis and therapeutic development. Here, we performed the first CZE-MS/MS-based quantitative top-down proteomics (TDP) of a small cohort of AD human brain samples and healthy controls (5 AD and 5 control) to determine the differentially quantified proteoforms between the two health conditions. Over 3000 proteoforms were identified, and only about 700 proteoforms were detected in both conditions, indicating drastically different proteoform profiles between the two conditions. The differentially quantified proteoforms (e.g., tau, neurogranin, and calmodulin-1 proteoforms) are associated with biological processes relevant to AD development, for example, amyloid fibril formation, microtubule disruption, synaptic transmission, and axogenesis. The results offer a deep view of the proteoform transformation in the AD human brain compared to the healthy control, providing potential proteoform biomarkers for AD diagnosis and proteoform targets for therapeutic development.
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