Abstract
The promotion of neurological recovery by enhancing neuroplasticity has recently obtained strong attention in the stroke field. Experimental studies support the hypothesis that stroke recovery can be improved by therapeutic interventions that augment neuronal sprouting. However plasticity responses of neurons are highly complex, involving the growth and differentiation of axons, dendrites, dendritic spines and synapses, which depend on the pathophysiological setting and are tightly controlled by extracellular and intracellular signals. Thorough mechanistic insights are needed into how neuronal plasticity is influenced by plasticity-promoting therapies in order not to risk the success of future clinical proof-of-concept studies.
Highlights
Following ischemic stroke, neuronal networks in the vicinity and at distance to the stroke are reorganized
In view of the robust evidence that neurological recovery may be stimulated by therapeutic interventions that enhance neuronal plasticity, there is considerable hope that we may soon become able to use those therapies for enhancing neurological recovery in stroke patients
For a proper idea of drug actions, morphological and molecular insights are required in the preparation of clinical trials that identify substrates of neuronal plasticity, which are subsequently targeted in stroke patients
Summary
Neuronal networks in the vicinity and at distance to the stroke are reorganized. In contrast to acute neuroprotective therapies, plasticity-promoting therapies have proven efficacy over weeks or even months post-stroke in animal and human studies Within this perspective article, we would like to briefly integrate some findings regarding brain remodeling and plasticity after stroke, elucidating: (a) structural surrogates of successful neurological recovery depending on the localization of ischemic lesions; (b) reorganization and plasticity processes of the cellular, subcellular and network level; (c) critical time windows for various therapeutic interventions; and (d) modes for the delivery of biologicals or drugs. We will shortly present (e) selected molecular signals that are likely mediators of plasticity processes, since we believe that understanding these signals is a major hallmark to prevent the failure of treatments in future clinical studies
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