MCP-1 and eotaxin-1 selectively and negatively associate with memory in MCI and Alzheimer's disease dementia

Brianne M Bettcher1, Ryan Fitch2, Matthew J Wynn2

  • 1Rocky Mountain Alzheimer's Disease Center, Departments of Neurosurgery and Neurology, University of Colorado Anschutz School of Medicine, Aurora, CA, USA; Memory and Aging Center, Department of Neurology, University of California, San Francisco, San Francisco, CA, USA.

Abstract

Insights

Elevated levels of monocyte chemoattractant protein-1 (MCP-1) and eotaxin-1 are linked to memory decline in mild cognitive impairment (MCI) and Alzheimer's disease (AD) dementia.

Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Monocyte chemoattractant protein-1 (MCP-1) and eotaxin-1, encoded on chromosome 17, are known to impair hippocampal neurogenesis in mice.
  • Investigating the specific association of these chemokines with memory deficits in human cognitive impairment is crucial.

Purpose of the Study:

  • To determine if MCP-1 and eotaxin-1 selectively correlate with memory impairment in individuals with mild cognitive impairment (MCI) and Alzheimer's disease (AD) dementia.
  • To explore the relationship between these chemokines and brain structure in affected individuals.

Main Methods:

  • Assayed MCP-1 and eotaxin-1 levels in control, MCI, and AD dementia patients (n=171).
  • Utilized magnetic resonance imaging (MRI) on a subset (n=55) to assess medial temporal lobe volumes.
  • Created composite cognitive scores and analyzed associations with chemokine levels and brain imaging data.

Main Results:

  • An interaction between MCP-1 and eotaxin-1 was observed, where elevated levels of both correlated with memory impairment.
  • These associations remained significant even after accounting for APOE genotype and other chemokines.
  • Elevated MCP-1 and eotaxin-1 predicted reduced left medial temporal lobe volume but did not impact other cognitive domains.

Conclusions:

  • MCP-1 and eotaxin-1 may play a selective role in memory dysfunction associated with MCI and AD dementia.
  • These findings highlight potential therapeutic targets for memory deficits in neurodegenerative diseases.