ArticleAlzheimer's research & therapy2025
Protein co-aggregates of dense core amyloid plaques and CSF differ in rapidly progressive Alzheimer's disease and slower sporadic Alzheimer's disease.
Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
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6 authors.
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Abstract
backgroundThe rapidly progressive phenotype of Alzheimer's disease (rpAD) remains a rare and less-studied entity. Therefore, the replication of key results from the rpAD brain and cerebrospinal fluid (CSF) is lacking.
methodsA label-free quantitative LC-MS/MS analysis of proteins co-aggregating with core-amyloid
resultsA total of 1841 proteins were characterized in the FFT study, of which 463 were consistently identified in every rpAD patient analyzed. One thousand two hundred eighty-three proteins were shared between the FFT and the prior FFPE study. FFT offered a more comprehensive proteomic profile than the prior FFPE study and prominently included the immune system pathways. Thirty-five proteins were shared in the FFT brain tissue, matched CSF from the same subjects, in which biological processes related to immune response were again notable. These results were validated against prior published proteomic CSF AD data with a faster rate of progression to identify the top 5 potential protein biomarkers of rapid progression in AD CSF.
conclusionsThese results support a distinct immune-related proteomic profile in both the brain and the CSF that can be explored as potential biomarkers in the future for the clinical diagnosis of rpAD.
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