Trends in Cognitive Sciences
OpinionAging cognition: from neuromodulation to representation
Section snippets
Cognitive aging phenomena at different levels
Since the first studies on adult age differences in intellectual functioning were published in the 1920s (e.g. Ref. 2), cognitive aging phenomena have been studied at various levels (see Fig. 1). At the behavioral level, individual difference researchers have documented aging-related declines in many psychometric measures of fluid intelligence 3 (i.e. basic cognitive mechanics 4 for memorizing, reasoning, and learning). Furthermore, aging-related increases of intra-individual variability,
Aging, information processing, and neuromodulation
Aging affects three main facets of information processing. People's abilities to activate, to represent and maintain information in mind, to attend to relevant but ignore irrelevant information, and to process information promptly decline with advancing age. At the neurobiological level, the efficacy of neuromodulation also declines. Among various neurotransmitter systems, we focus on the monoamines (e.g. serotonin and the catecholamines, particularly dopamine and noradrenaline) 15, 16, 17, 18,
Recent computational theories linking neuromodulation with cognitive aging
In 1990, two mathematical theories of cognitive aging were proposed in part to resolve the interdependence and circularity problems facing the resource-reduction theories 47, 48. Although not operating at the level of neuromodulation, both theories foreshadowed cross-level conceptual orientation. The network-disconnection theory of aging and information-processing rate 47 makes broad reference to neuroanatomical changes that might involve the degeneration of axonal connections. The
From deficient neuromodulation to neural noise
A classical hypothesis of cognitive aging at the neurobiological level is increased neural noise (haphazard activation during neuronal information processing) 50. However, thus far, mechanisms leading to such an increase and its proximal and distal consequences have not been unveiled. Simulating aging-related decline of dopaminergic neuromodulation by attenuating the G parameter in neural networks hints at a possible chain of mechanisms relating deficient neuromodulation to increased neural
Less distinctive cortical representations
The computational simulations further show that as reduced responsivity leads to increased intra-network random activation variability, another subsequent effect is a decrease in the distinctiveness of the network's internal representations. Low representational distinctiveness means that the activation profiles formed across the network's hidden units for different stimuli are less readily differentiable from each other. To illustrate this, Fig. 3c shows the internal activation patterns
Implications: a paradigm shift towards co-evolving fields across levels
Details regarding the involvement of neuromodulation in cognitive aging deficits remain to be unraveled. Pieces of the puzzle are emerging in various sub-fields, and the field as a whole could benefit from a paradigm shift towards overarching frameworks seeking to integrate cognitive aging phenomena across different levels. The proposed theoretical link – from attenuated neuromodulation to increased neural noise and less distinctive cortical representations in the aging brain, and finally on to
Acknowledgements
The authors are grateful to Valtteri Kassinen and Denise C. Park for permitting the redrawing of some data from their studies. We thank Todd S. Braver for helpful e-mail exchanges about the relations between his theory and ours. We are grateful to Naftali Raz, the anonymous reviewers, and Julia Delius for their many helpful comments on an earlier version of this article. We thank Peter A. Frensch for previous contributions to related work, and Paul B. Baltes and the Max Planck Institute for
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