Fibrinogen contributes to myelin deficit and cognitive impairment in aged mice after anesthesia and surgery
- Xueji Wang 1, Sufang Jiang 1, Tianyu Cao 1, Peiying Huang 1, Lichao Di 1, Jiaqi Li 1, Lining Huang 1,2,3
- Xueji Wang 1, Sufang Jiang 1, Tianyu Cao 1
- 1Department of Anesthesiology, The Second Hospital of Hebei Medical University, Hebei, China.
- 2Key Laboratory of Clinical Neurology, Ministry of Education, Hebei Medical University, Hebei, China.
- 3Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei, China.
- 0Department of Anesthesiology, The Second Hospital of Hebei Medical University, Hebei, China.
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August 7, 2025
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View abstract on PubMed
Summary
This summary is machine-generated.Fibrinogen in the brain after surgery causes myelin loss and cognitive issues in aged mice. Reducing fibrinogen levels reversed these effects, highlighting its role in perioperative neurocognitive disorder (PND).
Area Of Science
- Neuroscience
- Gerontology
- Anesthesiology
Background
- Perioperative neurocognitive disorder (PND) is a frequent complication after anesthesia and surgery, particularly in older adults.
- Fibrinogen's role in neurodegenerative disease suggests a potential link to PND pathogenesis.
Purpose Of The Study
- To investigate if fibrinogen contributes to myelin deficits and cognitive impairment in aged mice following anesthesia and surgery.
- To explore fibrinogen's impact on the central nervous system (CNS) and its potential as a therapeutic target for PND.
Main Methods
- Established a PND model in aged mice (17-month-old C57BL/6) using abdominal surgery.
- Assessed cognitive function and locomotion via behavioral tests.
- Utilized in vivo two-photon microscopy, immunostaining, electron microscopy, western blotting, and RT-qPCR to analyze CNS fibrinogen deposition, myelin integrity, oligodendrocyte status, and inflammation.
Main Results
- Anesthesia and surgery led to blood-brain barrier disruption and perivascular fibrinogen accumulation in the CNS.
- Fibrinogen deposition correlated with oligodendrocyte loss, reduced myelin sheath density, and behavioral abnormalities indicative of cognitive impairment.
- Fibrinogen depletion significantly reversed the myelin deficits and cognitive dysfunction observed in the PND model.
Conclusions
- Fibrinogen deposition in the CNS is a key factor in the early development of PND.
- Targeting fibrinogen may offer a therapeutic strategy to mitigate myelin damage and cognitive decline associated with anesthesia and surgery in elderly patients.
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