"Brain plasticity refers to the capacity of the nervous system to change its structure and its function over a lifetime, in reaction to environmental diversity. Although this term is now commonly used in psychology and neuroscience, it is not easily defined and is used to refer to changes at many levels in the nervous system ranging from molecular events, such as changes in gene expression, to behavior."
Neural Plasticity and Cognition
Structure and organization
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Neuroplasticity allows neurons to regenerate both anatomically as well as functionally, and to form new synaptic connections. Brain plasticity is the ability for the brain to recover and restructure itself. This adaptive potential of the nervous system allows the brain to recover after disorders or injuries and to reduce the effects of altered structures due to pathologies such as Multiple Sclerosis, Parkinson's disease, cognitive deterioration, Alzheimer's, dyslexia, ADHD, insomnia, etc.
Different teams of neurologists and cognitive psychologists that study the processes of synaptic plasticity and neurogenesis have shown that the battery of clinical exercises for brain stimulation designed by CogniFit encourages the creation of new synapses and neural circuits able to reorganize and recover the function of the damaged area and compensatory transmission capabilities. Researchers show that brain plasticity activated and strengthens applying this clinical intervention exercise program. See below an artistic representation of how continuous brain training may grow a neural network.
Neural networks before trainingNeural networks 2 weeks after stimulationNeural networks 2 months after stimulation
When engaged in new experiences and learning, the brain establishes a series of neural pathways. These neural pathways, or circuits, are routes made of inter-connecting neurons. These routes are created in the brain through daily use and practice; much like a mountain path is made by daily use of a shepherd and his herd. The neurons in a neural pathway communicate with each other through connections called synapses, and these communication pathways can regenerate throughout your whole life. Each time that we gain new knowledge (through repeated practice), the synaptic communication between neurons is strengthened. A better connection between the neurons means that the electric signals travel more efficiently when creating or using a new pathway. For example, when trying to recognize a new bird, new connections are made among specific neurons. Neurons in the visual cortex determine its color, the auditory cortex identifies its song, and other, the name of the bird. In order to know what bird it is, its attributes, its color, song, and name are repeated many times. Revisiting the neural circuit and re-establishing neuronal transmission between the implicated neurons at each new attempt enhances the efficiency of synaptic transmission. Communication between the relevant neurons is facilitated, cognition made faster and faster. Synaptic plasticity is perhaps the pillar on which the brain's amazing malleability rests.
Whereas synaptic plasticity is achieved through enhancing communication at the synaptic site between existing neurons, neurogenesis refers to the birth and proliferation of new neurons in the brain. For a very long time the notion of continued neuronal birth in the adult brain was considered heretic. Scientists believed that neurons died and were never substituted by new ones. Since 1944, but mostly in recent years, the existence of neurogenesis has become scientifically established and we know that it occurs when stem cells, a special type of cell located in the dentate gyrus, the hippocampus and possibly in the pre-frontal cortex, divide into two cells: a stem cell and a cell which will become a neuron fully equipped with axon and dentrites. Those new neurons will then migrate to distant areas of the brain where they are needed, and thus have the potential to allow the brain to replenish its supply of neurons. From animal and human research it is known that sudden neuronal death (for example after stroke) is a potent trigger for neurogenesis.
Functional Compensatory Plasticity
The neurobiological decline that accompanies aging is well documented in research literature and explains why older adults perform worse than young adults on tests of neurocognitive performance. Surprisingly, not all older adults exhibit lower performance. Some do as well as their younger counterparts. This unexpected behavioral advantage for a sub-group of aging individuals has been scientifically investigated and it was found that, when processing new information, higher performing older adults recruit the same brain regions as do the younger adults, but, also recruit additional brain regions that young and low performing older adults do not activate. Researchers have pondered on this over-recruitment of brain regions in high performing older adults and have generally reached the conclusion that recruitment of additional cognitive resources reflects a compensatory strategy. In the presence of age-related deficits and decreased synaptic plasticity which accompany aging, the brain, once again manifests its multi-source plasticity by re-organizing its neurocognitive networks. Studies show that the brain reaches this functional solution through the activation of alternative neural pathways, which most often activate regions in both hemispheres (when only one is activated in the younger adults).
Function and behavior: Learning, experience and the environment
We have seen that plasticity is the property of the brain which allows it to alter its biological, chemical and physical properties. However, as the brain changes, function and behavior are modified in a parallel course. In recent years we have learnt that cerebral alterations at the genetic or synaptic levels are brought about by a wide variety of environmental and experiential factors. New learning is at the heart of plasticity and an altered brain is perhaps the most tangible manifestation that new learning has occurred, which was made available by the environment. New learning occurs in many forms and for many reasons and at any time during our lifetime. For example, children acquire new knowledge in vast quantities and their brain changes significantly at these times of intensive new learning. New learning may also be required in the presence of neurological damage caused, for example through lesions or stroke, when the functions supported by a damaged brain area are impaired, and must be learnt anew. New learning can be intrinsic to the individual and guided by the thirst for knowledge. The multiplicity of circumstances for the occasion of new learning raises the question of whether the brain will change whenever it is learning something. Research suggests that this is not the case. It appears that the brain will acquire new knowledge, and thereby actualize its potential for plasticity, if the new learning is behaviorally appropriate. In order for learning to physiologically mark the brain, that learning must lead to changes in behavior. In other words new learning must be behaviorally relevant and necessary. For example new learning which ensures survival will be integrated by the organism and adopted as behavior and, as a result, the brain will have changed. Perhaps more important is the extent to which a learning experience is rewarding. For example, new learning in the form of interactive play is especially conducive of brain plasticity and was found to increase PFC activity. Also, in this context of incentive provision, we will note the time-old tradition of providing children with reinforcement and reward while they engage in learning.
Understanding the conditions for inducing plasticity
When, in the life span is the brain most likely to change when exposed to stimulation in the environment? It seems that plasticity patterns are different at different ages and much is still unknown regarding the interaction between the type of plasticity-inducing activity and the age of the subject. Nevertheless, we know that intellectual and mental activity induce brain plasticity when applied to healthy older adults or to older adults with a neurodegenerative disorder. More importantly, it appears that the brain is amenable to both positive and negative change even before the organism's birth. Animal studies show that when pregnant mothers are placed in enriched and stimulating environments, the offspring's synapse number increase in specific brain regions. Conversely, when light stress is applied to the pregnant mothers, her offspring later displayed a reduced PFC number of neurons. In addition, it appears that the PFC is more responsive to environmental influences than the rest of the brain. These findings have important implications for the "nature" vs. "nurture" debate, as it would appear that "nurture" may induce changes in neuronal gene expression. How does brain plasticity evolve and what is the effect of the length of time environmental stimulation is applied? This is a very important question for therapeutic issues and genetic animal research offers the very seminal answers that some genes are affected at even the shortest stimulation span, additional genes continue to be affected with longer stimulation span, while yet others undergo no change at all or reverse the changing trend. Although the mainstream use of the word plasticity carries a positive connotation, plasticity refers to all the ways the brain changes, and some of the changes may co-occur with impaired function and behavior. Cognitive training seems ideal for inducing cerebral plasticity. It provides the systematic practice necessary for establishing new neural circuits and for strengthening the synaptic connections among the neurons in the circuit. However, as we have seen, in the absence of a tangible behavioral benefit, the brain will not learn effectively. Thus, the importance of integrating highly personalized and relevant goals with the training cannot be overstated.
Definition adopted from: Kolb, B., Muhammad, A., & Gibb, R., Searching for factors underlying cerebral plasticity in the normal and injured brain, Journal of Communication Disorders (2010), doi:10.1016/j.jcomdis.2011.04.007