This study demonstrates that there is a lack of central memory formation in vitro in aged T cells in a model mouse system and that several factors contribute to this lack of new central memory formation in the T cells of the aged. This study shows that prior to culture the T cells of the aged contain an increased concentration of nitric oxide in comparison to the young. This increased amount of NO leads to an increased likelihood of cell death due to formation of peroxynitrite and other reactive oxygen and/or nitrogen species (ROS/RNI) in individual cells. Increased cell death means decreased chance of T cells contributing to new immunologic memory. Upon T cell receptor stimulation in the T cells of the aged, the increased NO and resultant increases in ROS/RNI lead to a greater likelihood of cell death. Increased death upon activation ultimately means fewer T cells from aged donors will survive to become new immunologic memory. This study also shows that this death pathway occurs relatively soon post-stimulation and, unlike other death pathways, is not reversible with IL-2 treatment. We also show that those few T cells of the aged able to survive activation and subsequent rounds of division are capable of becoming effector memory and eventually central memory T cells. The problem remains, though, that very few T cells of the aged do survive the initial activation and then progress through the 6 to 10 further rounds of division required to become a T cell of the central memory phenotype. This deficit of central memory formation is a very important concern in modern immunology and must be addressed in order to improve vaccine efficacy in the elderly.