Abstract
Existing neurocomputational and empirical data link deficient neuromodulation of the fronto-parietal and hippocampal-striatal circuitries with aging-related increase in processing noise and declines in various cognitive functions. Specifically, the theory of aging neuronal gain control postulates that aging-related suboptimal neuromodulation may attenuate neuronal gain control, which yields computational consequences on reducing the signal-to-noise-ratio of synaptic signal transmission and hampering information processing within and between cortical networks. Intervention methods such as cognitive training and non-invasive brain stimulation, e.g., transcranial direct current stimulation (tDCS), have been considered as means to buffer cognitive functions or delay cognitive decline in old age. However, to date the reported effect sizes of immediate training gains and maintenance effects of a variety of cognitive trainings are small to moderate at best; moreover, training-related transfer effects to non-trained but closely related (i.e., near-transfer) or other (i.e., far-transfer) cognitive functions are inconsistent or lacking. Similarly, although applying different tDCS protocols to reduce aging-related cognitive impairments by inducing temporary changes in cortical excitability seem somewhat promising, evidence of effects on short- and long-term plasticity is still equivocal. In this article, we will review and critically discuss existing findings of cognitive training- and stimulation-related behavioral and neural plasticity effects in the context of cognitive aging, focusing specifically on working memory and episodic memory functions, which are subserved by the fronto-parietal and hippocampal-striatal networks, respectively. Furthermore, in line with the theory of aging neuronal gain control we will highlight that developing age-specific brain stimulation protocols and the concurrent applications of tDCS during cognitive training may potentially facilitate short- and long-term cognitive and brain plasticity in old age.
Highlights
Normal aging is accompanied by alterations in multiple cognitive functions with negative consequences on various daily activities
Associative memory deficit (Li et al, 2005) as well as a range of other cognitive impairments commonly observed in old age could be accounted for by the aging neuronal gain control theory
We review existing findings of cognitive training and non-invasive brain stimulation interventions i.e., transcranial direct current stimulation and discuss their promises and constraints in activating the reduced but still available neurocognitive resources to buffer or ameliorate older adults’ cognitive functions
Summary
Normal aging is accompanied by alterations in multiple cognitive functions with negative consequences on various daily activities. The signal-to-noise ratio (SNR) of information processing is decreased in the simulated “old” network with a lower gain control, resulting in increased random processing fluctuations (Figure 1B), and attenuated rate (drift rate, v) of evidence accumulation (Figure 1C) Generalizing from these mechanisms, other simulation studies showed that the simulated “old network” exhibited less distinctive representations of activation patterns and less selective recruitment of specific processing modules that accounted for aging-related declines in working memory (Li and Sikström, 2002). According to the framework of the aging neuronal gain control theory (Li et al, 2001), reduced working memory and episodic memory capacity may stem from suboptimal DA modulation of the relevant networks, which may impair the SNR of information transfer within and between the respective brain circuitries, causing reduced specificity of information processing and less distinctive brain activation patterns. Evidence for why cognitive training and non-invasive brain stimulation can be seen as potential candidate interventions for promoting the aging brain’s neuronal gain control will be reviewed, alongside with critical discussions about the short- and long-term effects of these interventions
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