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APOE Isoforms Shape Microglia in Alzheimer’s Models
- A groundbreaking study reveals how APOE gene isoforms influence human microglia in Alzheimer’s pathology.
- APOE ε4 is a known genetic risk factor for Alzheimer’s, affecting gene expression and epigenomic states in microglia.
- Human microglia with different APOE isoforms were transplanted into an Alzheimer’s mouse model for analysis.
- APOE ε4 microglia showed elevated expression of pro-inflammatory genes, while ε3 focused on repair functions.
- APOE ε2 exhibited anti-inflammatory gene expression and supported neuroprotective pathways.
- APOE isoforms altered chromatin accessibility, influencing gene regulation in microglia under disease conditions.
- Understanding APOE’s role in microglial regulation opens avenues for precision medicine in neurodegenerative diseases.
- The study challenges previous views by positioning APOE as a key regulator of microglial gene networks.
- Research inspired by these findings may explore reversing APOE ε4-driven epigenetic changes for therapeutic benefits.
- Personalized treatments considering APOE genotype could optimize immunomodulatory therapies in Alzheimer’s.
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