A wide body of evidence shows that the Brain has a remarkable self-structured fitness to handle its abilities for modulating cognitive and motor skills after acute insults, during insidious neurodegenerative processes, psychological stress or even along the aging course. More recently, the term Resilience, which was originally borrowed from classic Mechanics studies of past Centuries, has been informally used to approach this fascinating subject. Permanent and transient lesions caused by strokes, tumors and concussions are studied to understand how the behavioral compensation following focal damage might be achieved after proper time and dependent on neural plastic changes such as axonal regeneration, sprouting and synaptic plasticity. From a genetic point of view, resilience might partially overlap with the concept of Penetrance and the widespread use of neuroimaging techniques surprisingly revealed that even the clinically asymptomatic carries for mutations or high genetic risk for neuropsychiatric conditions might often present anatomical or functional changes associated with disease progression or compensation mechanisms. Abnormal metabolic findings in the brains of asymptomatic carriers show that our definition of genetic penetrance based only on clinical parameters may be flawed, when dealing with hereditable movement disorders with probable metabolic endophenotypes. Curiously, a resilience mechanism modulated by the cerebellum has been recently considered in conditions like dystonia, familial idiopathic basal ganglia calcification and bipolar disorder. The fact that such affected regions may remain asymptomatic over several decades reveals a singular compensation mechanism, suggesting degeneracy of multiple neural systems. On the other hand, neuropsychology studies analyze Resilience as a cognitive and behavioral pattern of functioning and suggest that Epigenetics mechanisms, such as DNA methylation or histone acetylation might affect gene expression and ultimately the ability to cope with stressful events in both humans and animal models . However, so far, no resilience model explains completely the complexity of these intriguing findings. Imaging genetics is a promising strategy to integrate genotypic and phenotypic data and additional models of Brain functionality and efficiency suggests that theoretical models, such as the “small world” network might explain such clinical phenomenon. The thorough understanding of this process can only be achieved with a multidisciplinary and integrative approach, and a strong collaborative network that can build a new methodological paradigm to study brain resilience. As our understanding of this phenomenon improves, new therapeutic approaches may be planned to restore function by using alternative neuronal pathways in order to overcome damaged groups of neurons in the affected regions, fulfilling also crucial scientific gaps about brain self reorganization, and providing solid grounds for new diagnostic and therapeutic tools for neuropsychiatric disorders.
A wide body of evidence shows that the Brain has a remarkable self-structured fitness to handle its abilities for modulating cognitive and motor skills after acute insults, during insidious neurodegenerative processes, psychological stress or even along the aging course. More recently, the term Resilience, which was originally borrowed from classic Mechanics studies of past Centuries, has been informally used to approach this fascinating subject. Permanent and transient lesions caused by strokes, tumors and concussions are studied to understand how the behavioral compensation following focal damage might be achieved after proper time and dependent on neural plastic changes such as axonal regeneration, sprouting and synaptic plasticity. From a genetic point of view, resilience might partially overlap with the concept of Penetrance and the widespread use of neuroimaging techniques surprisingly revealed that even the clinically asymptomatic carries for mutations or high genetic risk for neuropsychiatric conditions might often present anatomical or functional changes associated with disease progression or compensation mechanisms. Abnormal metabolic findings in the brains of asymptomatic carriers show that our definition of genetic penetrance based only on clinical parameters may be flawed, when dealing with hereditable movement disorders with probable metabolic endophenotypes. Curiously, a resilience mechanism modulated by the cerebellum has been recently considered in conditions like dystonia, familial idiopathic basal ganglia calcification and bipolar disorder. The fact that such affected regions may remain asymptomatic over several decades reveals a singular compensation mechanism, suggesting degeneracy of multiple neural systems. On the other hand, neuropsychology studies analyze Resilience as a cognitive and behavioral pattern of functioning and suggest that Epigenetics mechanisms, such as DNA methylation or histone acetylation might affect gene expression and ultimately the ability to cope with stressful events in both humans and animal models . However, so far, no resilience model explains completely the complexity of these intriguing findings. Imaging genetics is a promising strategy to integrate genotypic and phenotypic data and additional models of Brain functionality and efficiency suggests that theoretical models, such as the “small world” network might explain such clinical phenomenon. The thorough understanding of this process can only be achieved with a multidisciplinary and integrative approach, and a strong collaborative network that can build a new methodological paradigm to study brain resilience. As our understanding of this phenomenon improves, new therapeutic approaches may be planned to restore function by using alternative neuronal pathways in order to overcome damaged groups of neurons in the affected regions, fulfilling also crucial scientific gaps about brain self reorganization, and providing solid grounds for new diagnostic and therapeutic tools for neuropsychiatric disorders.
