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Working memory (WM) performance is often decreased in older adults. Despite the growing popularity of WM trainings, underlying mechanisms are still poorly understood. Resistance to proactive interference (PI) constitutes a candidate process that contributes to WM performance and might influence training or transfer effects. Here, we investigated whether PI resistance can be enhanced in older adults using a WM training with specifically increased PI-demands. Further, we investigated whether potential effects of such a training were stable and entailed any transfer on non-trained tasks.
Healthy old adults (N = 25, 68.8 ± 5.5 years) trained with a recent-probes and an n-back task daily for two weeks. Two different training regimens (high vs. low PI-amount in the tasks) were applied as between-participants manipulation, to which participants were randomly assigned. Near transfer tasks included interference tasks; far transfer tasks assessed fluid intelligence (gF) or speed. Immediate transfer was assessed directly after training; a follow-up measurement was conducted after two months.
Both groups similarly improved in PI resistance in both training tasks. Thus, PI susceptibility was generally reduced in the two training groups and there was no difference between WM training with high versus low PI demands. Further, there was no differential near or far transfer on non-trained tasks, neither immediately after the training nor in the follow-up.
PI-demands in WM training tasks do not seem critical for enhancing WM performance or PI resistance in older adults. Instead, improved resistance to PI appears to be an unspecific side-effect of a WM training.
With imaging studies of recovery from stroke, it became clear that the brain retains a plastic potential in its motor and language domains not only in young rats or monkeys but also in adult humans and even in old and lesioned brains (Chollet et al., 1991; Weiller et al., 1992; 1995). This “reorganization” is individually highly variable (Weiller et al., 1993a), relates to recovery of lost function (Liepert et al., 1998), and can be influenced by drugs, training, and rehabilitation (Musso et al., 1999; Liepert et al., 2000a; Pariente et al., 2001). In our opinion, there is not just one single crucial component of recovery. Rather, recovery of function seems to imply the “reconnection” or perhaps better the “recoordination” of a network of areas, each of which may be specialized in one or more aspect of the lost function but requires the coherent and timely support from others to reach a high level of proficiency (Weiller and Rijntjes, 1999). Moreover, we can learn about how the normal brain works when looking at the diseased brain.
Brain anatomy of recovery from stroke
“Plastic” changes represent a uniform reaction pattern of the brain and occur under very different conditions in the intact as well as in the lesioned brain (Merzenich et al., 1982; Kaas, 1991) as a result of learning or adaptation, with or without any concomitant change in behavioral performance (Rijntjes et al., 1997). After lesions, plastic changes can either be a consequence of the structural defect (e.g. diaschisis) or a result of active intervention (e.g. rehabilitational procedures) (Weiller, 1998) In animal experiments, plastic changes have been demonstrated after recovery of lost motor function, including peri-lesional extensions of representations, shifts from primary to secondary parallel processing systems, and recruitment of homologous areas of the unaffected hemisphere (Fries et al., 1993; Nudo, 1997; Rouiller et al., 1998; Darian-Smith et al., 1999; Liu andRouiller, 1999). Such changes have also been identified in human stroke victims (Chollet et al., 1991; DiPiero et al., 1992; Weiller et al., 1992, 1993a; Seitz et al., 1994, 1998; Weder and Seitz, 1994; Binkofski et al., 1996; Dettmers et al., 1997).
In most studies using functional magnetic resonance imaging (FMRI) or positron emission tomography (PET), a widespread network of neurons was activated in both hemispheres after recovery.
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