Medical experts once believed that changes in the brain were only limited to infancy and childhood, after which its physical structure was permanent. However, we now know that new neural pathways are continuously being created and existing ones are altered as a part of our adaptation mechanism to new experiences, ongoing learning and the process of creating new memories.

This specific nature of the brain is called plasticity, also known as neuroplasticity. It refers to the brain's ability to self-modify its structure, function and chemistry due to internal or external changes. It has its roots in the Greek word "plastos," which means molded.

Plasticity can occur in response to learning activities that lead to new experiences and memory formation or in response to brain cell damage, when the brain rewires itself. The human brain has roughly 100 billion neuronal cells, with 2,500 synapses at birth growing in number to 15,000 synapses per neuron by age 3.

However, the number of synapses decreases to half in adulthood, due to their strengthening or weakening in relation to our experiences. This continuous branching and pruning of the synapses allows the brain to adapt to our ever-changing environment.

Brain plasticity is strong during infancy and childhood, but continues into adulthood as well. It has been clearly witnessed in the cases of recovery from brain injuries, sensory-motor deprivation due to stroke and peripheral injuries.

Likewise, it has been reported in aided function retrieval in prosthetic device users, artificial hearing and artificial sight. There have been an increasing number of studies in this area, and brain plasticity has been linked to various psychiatric and neurodegenerative disorders, including: stroke, Alzheimer's disease, Parkinson's disease and many psychological conditions, such as obsession, depression, compulsion and stress.

Perineuronal nets (PNNs) are specific structures that cover subsets of neurons in the central nervous system (CNS). They are basically specialized extracellular matrix molecules aggregated together and distributed in CNS. They appear relatively late in development. Their structures are nonstatic and reliant on the sensory experience, which highlights their involvement in neural plasticity regulation in early developmental period.

However, this mechanism of regulation is not fully understood. PNNs are involved in synapse stability, cellular relationship maintenance in the brain and various cellular functions, including neural plasticity. Furthermore, their role has been discussed in CNS pathological conditions, including: stroke, Alzheimer's disease, epilepsy and spinal cord injuries. This could lead to a great potential therapeutic application for PNNs in the post-injury nerve neural regeneration.

The organization and distribution of PNNs has been linked to appropriate sensory experience in early post-natal period. The major role of PNNs has been reported to be stabilizing the neuronal connectivity in order to restrict the plasticity and to minimize the plastic changes in effect of future sensory events. Therefore, PNN disruption could lead to CNS plasticity reactivation, along with activity-dependent changes, and finally neuronal connection reorganization.

Recent studies in mammalian systems have led to many interesting findings about PNNs. Briefly, it is believed that their enzymatic degradation after a CNS injury, like stroke, could enhance neuronal plasticity and help in functional recovery. Furthermore, there have been findings that show the therapeutic value of PNNs in other CNS dysfunctions, such as dementia and epilepsy.