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Ayanna Arneaud1, Serge Rivest2, Nataly Laflamme2

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Activating Nucleotide-binding oligomerization domain 2 (NOD2) with Muramyl Dipeptide (MDP) enhances amyloid-beta (AB) clearance in Alzheimer's disease models. Combining NOD2 activation with dexamethasone (Dex) synergistically boosts AB clearance and delays cognitive decline.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-beta (AB) accumulation and Cerebral Amyloid Angiopathy (CAA).
  • Monocytes are crucial for AB clearance, but their therapeutic role in CAA is underexplored.
  • NOD2 receptor activation by MDP shows potential for enhancing monocyte-mediated AB clearance.

Purpose of the Study:

  • To investigate the therapeutic potential of Nucleotide-binding oligomerization domain 2 (NOD2) activation by Muramyl Dipeptide (MDP) in enhancing AB clearance.
  • To evaluate the synergistic effects of MDP and dexamethasone (Dex) on monocyte modulation, AB efflux transporters, and cognitive function in Alzheimer's disease models.
  • To explore the underlying mechanisms of AB clearance modulated by NOD2 and glucocorticoids.

Main Methods:

  • Utilized wild-type, NOD2 knockout (KO), and APP/PS1 transgenic mouse models.
  • Assessed monocyte populations via flow cytometry and transporter expression (ABCB1, LRP-1) using western blot.
  • Evaluated cognitive function using the Novel Object Recognition Task.

Main Results:

  • MDP treatment shifted monocytes to an AB-clearing phenotype (Ly6Clow), an effect absent in NOD2 KO mice.
  • Dexamethasone (Dex) significantly upregulated ABCB1 and LRP-1 expression, enhancing AB efflux across the blood-brain barrier (BBB).
  • Combined MDP and Dex treatment demonstrated synergistic effects, improving transporter expression and delaying memory decline in APP/PS1 mice.

Conclusions:

  • NOD2 represents a promising therapeutic target for modulating innate immunity in AD and CAA.
  • Combining NOD2 activation with glucocorticoids offers a novel dual therapeutic strategy for AD and CAA.
  • This approach promotes both immune and BBB-mediated AB clearance while reducing neuroinflammation.