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Targeting foam cell formation to improve recovery from ischemic stroke
Jacob C Zbesko1, Jessica Stokes2, Danielle A Becktel1
1Department of Immunobiology, University of Arizona, United States.
Neurobiology of Disease
|April 17, 2023
Summary
Inflammation after ischemic stroke aids healing but causes neurodegeneration. Targeting lipid-filled foam cells may improve brain recovery and reduce cognitive deficits.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Inflammation is vital for healing after ischemic stroke but paradoxically exacerbates neurodegeneration and hinders regeneration for months.
- This chronic inflammation, particularly involving myeloid foam cells, contributes to delayed cognitive deficits in animal models.
- Foam cell formation results from overwhelmed myelin lipid clearance, driving persistent inflammation post-stroke.
Approach:
- This review synthesizes current knowledge on brain inflammation and foam cell development following ischemic stroke.
- It examines the mechanisms behind foam cell formation and their role in chronic inflammation.
- The review identifies potential therapeutic targets for intervention.
Key Points:
- Myeloid foam cells are key players in chronic stroke inflammation due to impaired lipid clearance.
- These foam cells are a major driver of the detrimental inflammatory response.
- Targeting lipid accumulation in foam cells presents a promising therapeutic strategy.
Conclusions:
- Understanding foam cell biology is critical for developing new stroke treatments.
- Interventions aimed at reducing lipid burden in foam cells could enhance neuroprotection and recovery.
- Further research into foam cell pathways may unlock novel therapeutic avenues for ischemic stroke.
