Objective:

To explore the role of microglia in Alzheimer's disease and propose therapeutic strategies that adjust microglial states and immune-metabolic interactions.

Approach:

Key Findings:

• Anti-Aβ monoclonal antibodies show statistically significant disease-modifying effects but limited cognitive improvement.
• Microglia are central to Alzheimer's disease susceptibility and progression, influenced by genetic and environmental factors.
• The traditional M1/M2 polarization model is inadequate; microglia exist in dynamic states influenced by various factors, as highlighted in the source.

Interpretation:

Future therapies for Alzheimer's disease should integrate both pathology removal and microenvironment protection, tailored to individual patient profiles, as suggested in the source.

Limitations:

• Current therapeutic strategies for adjusting microglial states remain unproven, as stated in the source.
• The complexity of microglial states and their interactions with various factors complicates treatment approaches.

Conclusion:

A shift in therapeutic focus from amyloid clearance to microglial state calibration is suggested in the source for effective Alzheimer's disease management.

Attribution Notice

This content is an AI-generated, fully rewritten summary based on a published scholarly article. It does not reproduce the original text and is not a substitute for the original publication. Readers are encouraged to consult the source for full context, data, and methodology.