Abstract
Purpose :
Chronic systemic inflammation associated with aging contributes to the development of various age-related diseases and enhances susceptibility to illnesses. Optic nerve damage is a prevalent cause of blindness, triggering inflammatory responses in both the nerve and retina. This study explores the impact of age on inflammation and its effects on optic nerve degeneration and retinal ganglion cell apoptosis.
Methods :
Young adult BL6/J mice (3-5 months) and aged counterparts (12-15 months) were divided into two groups, sacrificed two weeks and six months after crush injury. Confocal microscopy was employed for immunostaining optic nerves and retinas to assess scar formation and immune cell infiltration. Different markers were utilized to identify the distribution and types of immune cells.
Results :
Aged mice exhibited significant secondary degeneration in the optic nerve following injury. Apart from the crush site, multiple areas in the optic nerve lacking Glial Fibrillary Acidic Protein (GFAP) expression were identified. These regions were populated with CD68-positive and Oil Red O-positive foamy macrophages.
Conclusions :
The findings indicate heightened macrophage activation and a pronounced immune response to optic nerve injury in aged mice. Understanding these age-related differences in response to optic nerve injury is crucial for developing therapeutics tailored to the aging population.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.