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CSF Apo-E levels associate with cognitive decline and MRI changes.

Jon B Toledo1, Xiao Da, Michael W Weiner

  • 1Department of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, HUP, Maloney 3rd, 36th and Spruce Streets, Philadelphia, PA, 19104-4283, USA.

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Summary
This summary is machine-generated.

Higher cerebrospinal fluid Apo-E levels may protect against Alzheimer's disease (AD) progression, particularly in individuals without the APOE ε4 allele. This suggests a potential neuroprotective role for Apo-E proteins in AD pathogenesis.

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Apolipoprotein E (APOE) ε4 allele is a major genetic risk factor for Alzheimer's disease (AD).
  • APOE ε4 is thought to influence AD by altering apolipoprotein E (Apo-E) levels and amyloid-β (Aβ) clearance.
  • Limited data exists on the clinical and biomarker associations of Apo-E proteins.

Purpose of the Study:

  • To investigate the relationship between cerebrospinal fluid (CSF) and plasma Apo-E protein levels, APOE genotype, and cognitive/biomarker changes in AD.
  • To explore the potential neuroprotective role of Apo-E in AD.

Main Methods:

  • Analysis of CSF and plasma Apo-E levels in 311 and 565 subjects from the AD Neuroimaging Initiative, respectively.
  • Correlating Apo-E levels with cognitive function, CSF AD biomarkers (tau, Aβ), and gray matter atrophy.
  • Stratified analysis based on APOE genotype.

Main Results:

  • Higher CSF Apo-E levels correlated with increased CSF tau and were associated with cognitive decline and gray matter atrophy, independent of AD biomarkers.
  • These associations were significant only in individuals without the APOE ε4 allele.
  • Plasma Apo-E levels showed weak correlation with CSF Apo-E and no association with cognitive or MRI changes.

Conclusions:

  • Increased CSF Apo-E2 or -E3 levels may indicate a protective response in AD, potentially offering neuroprotection independent of tau and amyloid pathology.
  • CSF Apo-E levels, particularly in non-ε4 carriers, may serve as a biomarker for AD progression and neuroprotection.