Exploratory Assessment of Proteomic Network Changes in Cerebrospinal Fluid of Mild Cognitive Impairment Patients: A Pilot Study


Journal article


A. Kamalian, Sara Ho, Megha Patel, Alexandria Lewis, A. Bakker, M. Albert, Richard O'Brien, A. Moghekar, M. Lutz
Biomolecules, 2023

Semantic Scholar DOI PubMedCentral PubMed
Cite

Cite

APA   Click to copy
Kamalian, A., Ho, S., Patel, M., Lewis, A., Bakker, A., Albert, M., … Lutz, M. (2023). Exploratory Assessment of Proteomic Network Changes in Cerebrospinal Fluid of Mild Cognitive Impairment Patients: A Pilot Study. Biomolecules.


Chicago/Turabian   Click to copy
Kamalian, A., Sara Ho, Megha Patel, Alexandria Lewis, A. Bakker, M. Albert, Richard O'Brien, A. Moghekar, and M. Lutz. “Exploratory Assessment of Proteomic Network Changes in Cerebrospinal Fluid of Mild Cognitive Impairment Patients: A Pilot Study.” Biomolecules (2023).


MLA   Click to copy
Kamalian, A., et al. “Exploratory Assessment of Proteomic Network Changes in Cerebrospinal Fluid of Mild Cognitive Impairment Patients: A Pilot Study.” Biomolecules, 2023.


BibTeX   Click to copy

@article{a2023a,
  title = {Exploratory Assessment of Proteomic Network Changes in Cerebrospinal Fluid of Mild Cognitive Impairment Patients: A Pilot Study},
  year = {2023},
  journal = {Biomolecules},
  author = {Kamalian, A. and Ho, Sara and Patel, Megha and Lewis, Alexandria and Bakker, A. and Albert, M. and O'Brien, Richard and Moghekar, A. and Lutz, M.}
}

Abstract

(1) Background: Despite the existence of well-established, CSF-based biomarkers such as amyloid-β and phosphorylated-tau, the pathways involved in the pathophysiology of Alzheimer’s disease (AD) remain an active area of research. (2) Methods: We measured 3072 proteins in CSF samples of AD-biomarker positive mild cognitive impairment (MCI) participants (n = 38) and controls (n = 48), using the Explore panel of the Olink proximity extension assay (PEA). We performed group comparisons, association studies with diagnosis, age, and APOE ε4 status, overrepresentation analysis (ORA), and gene set enrichment analysis (GSEA) to determine differentially expressed proteins and dysregulated pathways. (3) Results: GSEA results demonstrated an enrichment of granulocyte-related and chemotactic pathways (core enrichment proteins: ITGB2, ITGAM, ICAM1, SELL, SELP, C5, IL1A). Moreover, some of the well-replicated, differentially expressed proteins in CSF included: ITGAM, ITGB2, C1QA, TREM2, GFAP, NEFL, MMP-10, and a novel tau-related marker, SCRN1. (4) Conclusion: Our results highlight the upregulation of neuroinflammatory pathways, especially chemotactic and granulocyte recruitment in CSF of early AD patients.



Tools
Translate to