Abstract:

A recent demographic shift towards increased age at time of spinal cord injury (SCI), as well as decreased functional recovery following SCI in older populations, create the need to investigate how age effects SCI pathology and repair. While decreased neuroplasticity or physical strength with age may contribute to functional deficits, work from our lab and others have identified exacerbated acute inflammatory events as contributors to age-dependent secondary injury. Specifically, our recent paper identified that increased production of reactive oxygen species (ROS) from macrophage nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) with age exacerbates secondary injury after SCI. Collectively, we identified ROS as instrumental in worsening functional outcomes following aged SCI and demonstrated that the therapeutic efficacy of ROS based treatments is age-dependent. This short review focuses on the role of age on worsening functional outcomes following SCI and provides a mechanistic overview into how age exaggerates secondary injury.