Peripheral nerve injury (PNI) affects millions of people worldwide, and regeneration of damaged peripheral axons is worse with advancing age. A decline in the functions of Schwann cells (SCs) and resident and infiltrating macrophages (MΦs) may contribute to the worsened regenerative capacity of the damaged aged peripheral nervous system (PNS). These cells are critical for effective PNS regeneration due to their release of neurotrophic factors and cell adhesion molecules (SCs), and phagocytosis of myelin and neuronal debris (MΦs and SCs). Our lab has shown an age-related decline in the expression of a small heat shock protein called alphaB-crystallin (αBC) that is expressed by SCs and axons. This reduction correlated with defective myelination and lipid synthesis in the injured PNS, as well as an increased presence of MΦs. The present thesis examined injury in the aged peripheral nerve at the gene level and how aging and injury impacted the expression of enzymes in the cholesterol biosynthesis pathway and, the presence and properties of SCs and MΦs. The possible contribution of αBC to age-related declines in injury responses was also assessed using mice null for the protein. At the gene level, cholesterol biosynthesis displayed certain patterns of down-regulation after injury as well as with age. Also, fewer SCs and MΦs were seen within the nerve with aging while MΦs from aged nerves potentially displayed deficits in debris clearance after injury. With respect to αBC, no consistent pattern of altered expression in genes associated with cholesterol biosynthesis nor SC numbers were evident in αBC knockout mice. However, older αBC null animals had more myelin debris-laden pro-inflammatory MΦs in later post-injury timepoints. Therefore, with increasing age, the natural decline in αBC may result in an increased presence of pro-inflammatory macrophages that could contribute to adverse symptoms. Future studies should explore possible deficits in MΦ lipid trafficking and clearance in the presence or absence of αBC.