The phenomenon of cognitive resilience, that is, the dynamical preservation of normal functions despite neurological disorders, demonstrates that cognition can be highly robust to devastating brain injury. Here, cognitive resilience is considered across a range of neurological conditions. Simple computational models of structure-function relationships are used to discuss hypotheses about the neural mechanisms of resilience. Resilience expresses functional redundancies in brain networks and suggests a process of dynamic rerouting of brain signals. This process is underlined by a global renormalization of effective connectivity, capable of restoring information transfer between spared brain structures via alternate pathways. Local mechanisms of synaptic plasticity mediate the renormalization at the lowest level of implementation, but it is also driven by top-down cognition, with a key role of self-awareness in fostering resilience. The presence of abstraction layers in brain computation and networking is hypothesized to account for the renormalization process. Future research directions and challenges are discussed regarding the understanding and control of resilience based on multimodal neuroimaging and computational neuroscience. The study of resilience will illuminate ways by which the brain can overcome adversity and help inform prevention and treatment strategies. It is relevant to combating the negative neuropsychological impact of aging and fostering cognitive enhancement. 1. Introduction In neurology, one is often faced with a relative disconnect between the clinical presentation and the underlying neuropathology or amount of brain damage [1–10]. One observes cognitive functions that appear to be relatively preserved in spite of damage to brain systems that one would expect to be normally implicated in these functions. Patients with similar brain damage or neurological disorder often show quite different neuropsychological profiles, with different evolutions, and cliniconeuropathological relationships are characterized by a strong between-subject variability [2, 9]. Part of this between-subject variability is underlined by static intrinsic differences in structure-function relationships in different subjects, for example, the lateralization of language, which makes certain patients less susceptible than others to certain impairments for similar brain damage, for example, damage to the left hemisphere, in which many critical functions for language are most often implemented in humans. Part of the variability is related to processes of recovery that
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