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Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
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Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

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Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer's Disease

Eunshil Lee1, Yongmin Chang1,2,3

  • 1Institute of Biomedical Engineering Research, Kyungpook National University, Daegu 41944, Republic of Korea.

Cells
|February 12, 2025
PubMed

Insights

Alzheimer's disease involves amyloid beta (Aβ) and neuroinflammation. Microglia play a dual role, complicating treatment. Understanding these interactions is key for new Alzheimer's therapies.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) pathology involves amyloid beta (Aβ) accumulation.
  • Neuroinflammation, mediated by microglia, plays a critical role in AD progression.
  • Microglia exhibit dual roles in neurodegeneration and neuroprotection, impacting AD pathogenesis.

Purpose of the Study:

  • To elucidate the complex interactions between Aβ protein, microglia, and neuroinflammation in AD.
  • To investigate the receptors and pathways involved in microglial activation in AD.
  • To enhance understanding of how microglial activation impacts and can be regulated within AD neuroinflammation.

Main Methods:

  • Comprehensive review of existing literature on Aβ, microglia, and neuroinflammation in AD.
  • Analysis of ongoing clinical trials investigating therapeutic targets in AD.
  • Examination of receptors and signaling pathways mediating microglial responses.

Main Results:

  • Aβ accumulation activates microglia, initiating neuroinflammatory responses.
  • Microglia secrete both pro-inflammatory and anti-inflammatory mediators, influencing neuronal fate.
  • The dual role of microglia complicates therapeutic strategies for AD.

Conclusions:

  • Understanding the intricate interplay between Aβ, microglia, and neuroinflammation is crucial for AD treatment development.
  • Targeting microglial activation pathways offers potential therapeutic avenues for AD.
  • Further research into neuroinflammation regulation may lead to therapies slowing AD progression.
Keywords:
Alzheimer’s diseasemicroglianeuroinflammationpathwaysreceptors

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