A deficiency in CCR2+ monocytes: the hidden side of Alzheimer's disease

Gaëlle Naert1, Serge Rivest

  • 1Neuroscience Laboratory, CHU de Québec Research Center and Department of Molecular Medicine, Faculty of Medicine, Laval University, 2705 Laurier Boulevard, Québec, QC, Canada G1V 4G2.

Insights

Bone marrow-derived microglia (BMDM) show neuroprotective functions in Alzheimer's disease (AD) by restricting amyloidosis. Impaired recruitment of CCR2(+) monocytes, essential for BMDM, is linked to AD progression.

Area of Science:

  • Neuroscience
  • Immunology

Background:

  • Alzheimer's disease (AD) involves amyloid-β (Aβ) plaques and neurofibrillary tangles.
  • Microglia play dual roles in AD, potentially clearing Aβ or secreting neurotoxins.
  • Recent research highlights distinct functions of resident and bone marrow-derived microglia (BMDM).

Purpose of the Study:

  • To review the current understanding of CCR2(+) monocyte roles in AD.
  • To explore the dysfunctions of CCR2(+) monocytes in Alzheimer's disease.
  • To identify CCR2(+) monocytes as potential therapeutic targets for AD.

Main Methods:

  • Review of existing literature on microglia and monocyte involvement in AD.
  • Analysis of studies investigating CCR2(+) monocyte recruitment and function.
  • Synthesis of findings on the neuroprotective and amyloid-restricting capabilities of BMDM.

Main Results:

  • BMDM are identified as the primary cell type restricting cerebral amyloidosis in AD.
  • CCR2(+) monocytes are crucial for the beneficial functions of BMDM.
  • Impaired CCR2(+) monocyte recruitment is observed in AD patients, indicated by monocytopenia.

Conclusions:

  • CCR2(+) monocytes and their recruitment are critical for neuroprotection in AD.
  • Dysfunctional CCR2(+) monocyte pathways represent a significant aspect of AD pathogenesis.
  • Targeting CCR2(+) monocyte pathways offers a promising therapeutic strategy for Alzheimer's disease.

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