In young controls, the AST elicits longer latencies and a higher incidence of directional errors than the prosaccade task (PST). In older adults, these differences are inflated (e.g., Eenshuistra et al., 2004; Crawford et al., 2005; Butler and Zacks, 2006; Peltsch et al., 2011). Despite the prevalence of AST impairments in older adults, the source of these impairments remains unclear. An increased AST latency and the higher error rate found in older adults have been interpreted as a typical age-related decline of inhibitory function (Klein et al., 2000; Sweeney et al., 2001; Peltsch et al., 2011). In agreement with research on the decline of IC with age (Raemaekers et al., 2006; Peltsch et al., 2011), Alichniewicz et al. (2013) demonstrated the reduced ability of older adults to voluntarily inhibits saccadic responses compared to young adults. Additionally, the onset latencies of both prosaccades and antisaccades were significantly longer in healthy older adults, compared to their young counterparts. WM capacity is also suggested to account for the difference between younger and older adults in the AST (Eenshuistra et al., 2004; Crawford et al., 2013). For example, the observed age-related AST impairments could be influenced by declining WM capacity (Baltes et al., 1999), declining levels of activation of task goals, and/or rates of refreshment of crucial task information in WM (e.g., Duncan et al., 1996; Nieuwenhuis et al., 2004), or declining inhibitory efficiency in controlling the amount of task-irrelevant information entering, remaining in, and being filtered out of, WM (e.g., Hasher and Zacks, 1988; Hasher et al., 1999). The accounts differ in the extent to WM (or IC) decline is considered to be a direct source of AST impairments, rather than an indirect, emergent property of cognitive impairment.