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Basic Science and Pathogenesis.

Artur Shvetcov1,2,3, Heather M Wilkins4,5,6, Jeffrey M Burns4,5

  • 1Discipline of Psychiatry and Mental Health, University of New South Wales, Sydney, NSW, Australia.

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PubMed
Summary
This summary is machine-generated.

Apolipoprotein E ε4 (APOE4) carriers show a distinct proteome signature in cerebrospinal fluid and plasma, regardless of cognitive status. This signature, linked to apoptosis and inflammation, indicates systemic changes that may increase vulnerability to Alzheimer's disease (AD) and mild cognitive impairment (MCI).

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Area of Science:

  • Neuroscience
  • Genetics
  • Proteomics

Background:

  • Apolipoprotein E ε4 (APOE4) is the primary genetic risk factor for Alzheimer's disease (AD) and mild cognitive impairment (MCI).
  • Mechanisms underlying APOE4 carrier vulnerability remain largely unknown.

Purpose of the Study:

  • To identify proteomic differences associated with APOE4 carriage.
  • To investigate the biological pathways affected by APOE4.

Main Methods:

  • Utilized the Global Neurodegeneration Proteomics Consortium dataset (8965 NI, 1283 AD, 505 MCI).
  • Employed SomaScan 7k assay for plasma and cerebrospinal fluid (CSF) proteomic data.
  • Applied mutual information and classification and regression trees (CART) for feature selection and machine learning.
  • Conducted functional network analyses to identify associated biological pathways.

Main Results:

  • APOE4 carriers exhibited a unique proteome signature in both CSF and plasma, independent of cognitive status (NI, MCI, AD).
  • APOE4-specific proteins were associated with apoptosis, inflammation, immune system DNA/RNA processes, mitochondrial organization, and glycolysis.

Conclusions:

  • APOE4 carriage significantly influences the proteome in both CSF and plasma, indicating systemic biological alterations.
  • These alterations are necessary but not sufficient for MCI and AD development, potentially increasing vulnerability to environmental factors.
  • Findings suggest APOE4-driven biological changes combined with environmental insults may drive AD and MCI pathogenesis.