Brain recovery – towards an unified theory

the large body of evidence we have today, for reorganization , repair and functional recovery after injury, the underline mechanisms for these combined processes are still unclear. This " blind spot " has negative impact on development of treatment strategies in the near future. To solve this issue, it is not easy to reconcile divergent opinions, despite all new available research technologies: some scientists would argue for a precise localiza-tion of brain functions in specific areas, others would hypothesize that different functions are more widely distributed throughout the brain. Some critical points of view regarding this general concept stated that recovery of function in neurological diseases in fact does not exist. These suggest that only one type of compensation exists [1]. In this context, plasticity is defined by the extent to which such alleviation is possible. Taking into consideration the data from many fMRI and PET scanning studies, as well as from studies showing discrepancy between functional consequences of acute versus chronic lesions [2] and the classic example of " serial lesion effect " [3], it appears that more arguments favour the theory that brain functions are widely distributed and in constant dynamic change [4–6]. It seems also that CNS has an equipotentiality of vicarious functions. Nowadays, we generally accept the idea that dynamic neuronal networks reorganization is permanently active and not only a characteristic of the damaged brain. After constant negative results in translating data from basic to clinical trials for neuropro-tection, in stroke, traumatic brain injury and other neurological conditions, we acknowledge that a shift of strategy in development of pharmacological treatments is needed [7]. A deeper understanding of brain functioning and pathophysiological processes is mandatory in this respect. Regarding brain biology today, we have learned that neu-rotrophicity, neuroprotection, neuroplasticity and neurogenesis are the key endogenous neurobiological processes that act together under genetic control to generate endogenous defence activity (EDA), which attempts to counteract pathophysiological processes [8]. These fundamental neurobiological processes lack absolute boundaries; they overlap and share common mechanisms in such a way that they cannot be separated within the continuum of EDA [9]. EDA can be endogenously or pharmacologically activated. Furthermore, neurobiological processes of EDA share common mechanisms with pathophysiological processes. For example, excitotoxicity, neurotrophicity and neuroplasticity all have NMDAR stimulation as their common important driver [10, 11]. Inflammation is another important contributor to neu-roregeneration, stimulating neuroplasticity via trophic factors [12–16]. Regulation disturbances in each of …