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Neurosciences

Aging Impairs Angiogenic Support for Peripheral Nerve Regeneration

Strategic Insights

— 1 min read

Aging is known to impair the physiologic ability of peripheral nerves to regenerate after injury, a phenomenon that is still incompletely characterized. Research on senescence-accelerated mice has revealed that aging influences the intraneural angiogenic response that occurs after injury and during regeneration of peripheral nerves. The study found that old and senescence-accelerated mice are unable to locally upregulate vascular endothelial growth factor (VEGF), a prototypical angiogenic cytokine, after injury, and have substantial deficits in mounting an appropriate intraneural angiogenic response during nerve regeneration.

Key Takeaways:

  • Aging impairs the ability of peripheral nerves to regenerate after injury, with mechanisms still incompletely characterized.
  • The intraneural angiogenic response that occurs after injury and during regeneration of peripheral nerves is influenced by aging.
  • Old and senescence-accelerated mice are unable to locally upregulate VEGF, a prototypical angiogenic cytokine, after injury.
  • These mice have substantial deficits in mounting an appropriate intraneural angiogenic response during nerve regeneration.
  • The findings suggest interdependent relationships between aging, VEGF, angiogenesis, and nerve regeneration and imply vascular abnormalities may play a role in aging-associated neurological dysfunction.
  • R. Pola and colleagues at Tufts University, School of Medicine conducted the study and published their findings in Neurobiology of Aging.

Statistics:

  • 25(10):1361-1368 is the page range for the published study in Neurobiology of Aging.
  • 1361 is the starting page number for the study.
  • 1368 is the ending page number for the study.
  • 10 is the volume number for the study in Neurobiology of Aging.
  • VEGF (vascular endothelial growth factor) is a prototypical angiogenic cytokine reduced in old and senescence-accelerated mice.

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Sources:

  • Neurobiology of Aging (2004;25(10):1361-1368)
  • R. Pola et al., Tufts University, School of Medicine.

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