Fibrinogen contributes to myelin deficit and cognitive impairment in aged mice after anesthesia and surgery.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study assessing biological mechanisms
PubMed 40770921 · doi:10.1177/0271678X251338953
What was done
Seventeen-month-old C57BL/6 mice underwent abdominal surgery under anesthesia to establish a model of perioperative neurocognitive disorder (PND). Blood-derived fibrinogen accumulation in the central nervous system following blood-brain barrier disruption was tracked with in vivo two-photon brain microscopy. Myelin sheath density and oligodendrocyte changes were evaluated via immunostaining, electron microscopy, and western blotting. Inflammatory markers were measured with RT-qPCR, and cognitive and locomotor behaviors were tested before and after fibrinogen depletion.
What was found
The abstract reports no numerical data, baseline values, or statistical significance levels. Anesthesia and surgery induced blood-brain barrier disruption and fibrinogen accumulation in the central nervous system, leading to oligodendrocyte loss, myelin deficits, and behavioral impairments. Fibrinogen depletion reversed these post-surgical myelin deficits and cognitive declines.
Why it matters
The study identifies blood-derived fibrinogen leakage as a mechanistic contributor to demyelination and cognitive decline after surgery, suggesting a candidate pathway for interventions targeting perioperative neurocognitive disorders.
Limits
Findings are limited to an animal model and cannot be directly assumed in human perioperative settings. The abstract does not report sample sizes, specific quantitative effect sizes, or the exact pharmacological or genetic method used for fibrinogen depletion.
Cited by
- supports Systemically lowering fibrinogen in mouse models of blood-brain barrier dysfunction reduced brain fibrinogen leakage and partially restored cerebral blood flow and barrier integrity.