Traumatic brain injury (TBI) is a leading cause of death and poses significant challenges for elderly populations, often exacerbating existing cognitive decline. Empirical evidence suggests disruptions in cholinergic neurotransmission following TBI may contribute to cognitive deficits. We predicted that parietal injury in aged (15-16 months old) male rats will augment sustained attention deficits compared to young adults. We then hypothesized that chronic NS-1738, a novel positive allosteric modulator (PAM) of the α7 nicotinic ACh receptor (α7-NAChR) will improve sustained attention post-TBI in aged rats, alone and in combination with environmental enrichment (EE). Aged male rats were trained in the 3-choice serial reaction time task (3-CSRT) prior to injury and required more sessions to reach criterion than young adults. Following a controlled cortical impact (CCI) of moderate severity to the right parietal lobe or sham injury, rats were randomized to daily NS-1738 (5 mg/kg) or vehicle, as well as daily EE (24h) or standard housing starting post-injury day (PID) 1. 3-CSRT retrials occurred on PID 17-27. Anxiety-like behavior was assessed via the open field test (OFT) on PID 28. Cortical lesion volumes were assessed post-sacrifice. Statistical analysis utilized repeated measures ANOVAs with Newman-Keuls post hoc tests. TBI-induced cognitive deficits were pronounced in aged rats (p<0.05) and were rescued by chronic NS-1738 (p<0.05). NS-1738+EE rendered an additive effect on restoring accuracy and lowering omissions (p<0.05). TBI reduced OFT center exploration without reductions in ambulation (p<0.05). NS-1738 and EE housing individually restored center exploration (p<0.05). While both NS-1738 and EE rendered trends in reducing the extent of cavitation, the combined therapy was ineffective at promoting tissue preservation. Our findings reflect the vulnerability of the elderly following TBI and support benefits of α7-NAChR PAM and/or EE treatment after experimental brain trauma on sustained attention through cholinergic neurotransmission.