Aging exacerbates development of cerebral microbleeds in a mouse model
Rachita K Sumbria1,2, Mher Mahoney Grigoryan2, Vitaly Vasilevko3
1Department of Biopharmaceutical Sciences, School of Pharmacy, Keck Graduate Institute, Claremont, CA, USA.
Journal of Neuroinflammation
|March 8, 2018
Summary
Aging increases susceptibility to inflammation-induced cerebral microhemorrhages (CMH) in mice. This heightened risk is linked to greater microglial/macrophage activation in older brains, impacting CMH development.
Area of Science:
- Neuroscience
- Immunology
- Aging Research
Background:
- Cerebral microhemorrhages (CMH), the MRI-visible cerebral microbleeds (CMB), are common in aging brains.
- Systemic inflammation's role in CMH is recognized, but its interplay with aging remains unclear.
- This study investigates age-dependent differences in inflammation-induced CMH pathogenesis.
Purpose of the Study:
- To determine if age influences the development of inflammation-induced CMH in mice.
- To explore the relationship between aging, systemic inflammation, and CMH development.
- To examine age-related changes in neuroinflammation and blood-brain barrier integrity in response to lipopolysaccharide (LPS).
Main Methods:
- Young and old C57BL/6 mice were injected with low-dose lipopolysaccharide (LPS) or saline.
- Brains were analyzed for acute/fresh (H&E) and sub-acute (Prussian blue) CMH.
- Immunohistochemistry assessed microglial/macrophage activation, astrocyte activation, and blood-brain barrier (BBB) disruption.
Main Results:
- Aging alone did not increase spontaneous CMH but significantly exacerbated LPS-induced CMH.
- Aged mice exhibited larger CMH, with increased microglial/macrophage activation correlating with CMH development.
- LPS-treated aged mice showed heightened astrocyte activation and BBB disruption compared to young mice.
Conclusions:
- The aging brain is more vulnerable to inflammation-induced CMH in mice.
- Increased CMH in aged mice is associated with elevated microglial/macrophage activation.
- Age potentiates neuroinflammatory responses and BBB breakdown following LPS challenge.
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