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AIBP controls TLR4 inflammarafts and mitochondrial dysfunction in a mouse model of Alzheimer's disease

Yi Sak Kim1, Soo-Ho Choi1, Keun-Young Kim2

  • 1Department of Medicine, University of California, San Diego, La Jolla, San Diego, CA, 92093, USA.

Journal of Neuroinflammation
|September 28, 2024
PubMed

Insights

ApoA-I binding protein (AIBP) protects against Alzheimer's disease by regulating microglia inflammatory responses and mitochondrial function. Loss of AIBP exacerbates neuroinflammation, oxidative stress, and neurodegeneration in mouse models.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia-driven neuroinflammation is critical in Alzheimer's disease (AD) pathogenesis.
  • Activated microglia form TLR4 inflammarafts, cholesterol-rich platforms for inflammatory signaling.
  • ApoA-I binding protein (AIBP) interacts with TLR4, targeting cholesterol depletion to inflammatory microglia.

Purpose of the Study:

  • To investigate the role of AIBP in regulating TLR4 inflammarafts and microglial function in Alzheimer's disease.
  • To determine the impact of AIBP deficiency on neuroinflammation, mitochondrial dynamics, and AD progression in a mouse model.

Main Methods:

  • In vitro studies using microglia exposed to amyloid-beta (Aβ).
  • In vivo studies using APP/PS1 transgenic mice with and without AIBP (Apoa1bp-/- APP/PS1).
  • Analysis of TLR4 inflammaraft formation, mitochondrial morphology, reactive oxygen species (ROS), endoplasmic reticulum dilation, Aβ plaque load, neuronal cell death, and animal survival.

Main Results:

  • Aβ induced TLR4 inflammaraft formation in microglia.
  • Apoa1bp-/- APP/PS1 microglia exhibited hyperbranched mitochondria, increased ROS, and ER dilation.
  • Aβ plaque burden and neuronal death were increased, while survival was decreased in Apoa1bp-/- APP/PS1 mice compared to controls.

Conclusions:

  • AIBP regulates TLR4 inflammarafts and mitochondrial dynamics in microglia.
  • AIBP plays a protective role against oxidative stress and neurodegeneration in Alzheimer's disease.
  • Targeting AIBP may offer a therapeutic strategy for Alzheimer's disease.
Keywords:
AIBPAlzheimer’s diseaseInflammaraftLipid raftsMicrogliaMitochondriaNeuroinflammationOxidative stressTLR4

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