Contrary to what was once popular belief, our daily experiences largely impact our neural network and brain structure, even through adulthood. Although our genes are responsible for a “first draft” of the brain, this is frequently revised and edited throughout our lives by the experiences we have. This brings us to the topic of neuroplasticity, formally defined as “the ability of the nervous system to change its activity in response to intrinsic or extrinsic stimuli by reorganizing its structure, functions, or connections”. This change in activity presents itself as a change in brain functional activity, or brain structure (for example a change in the volume of grey matter). To understand how neuroplasticity arises, we must look at two specific features of brain development: neural stem cells and dendrite plasticity. Stem cells lining the subventricular zone can form neurons when they are activated. Their activation is influenced by factors such as drugs, hormones, and injury, and is the reason we can observe ‘brain reorganization’ following intense brain trauma. Dendrites, on the other hand, show a remarkably rapid response to experience, sometimes forming synapses within minutes. This rapid response makes them an essential component in the brain’s malleability. Furthermore, an overproduction of neurons during brain development, followed by synaptic pruning (the removal of synapses) helps routinely fine tune the neural network based on which connections are used most often. Four main types of neuroplastic adaptations have been established: neurogenesis, synaptogenesis, long-term potentiation, and long-term depression.
Neurogenesis-the generation of new neurons by the division of neural stem cells into neural progenitor cells, and then the maturation of these progenitor cells into neurons
Synaptogenesis-the formation of new synapses, which is integral in creating a network of neural connections. This occurs when the brain is exposed to new experiences, activities, or environments.
Long-term potentiation-the strengthening of synapses through repeated exercise or activity (also known as synaptic plasticity). LTP is associated with learning and memory and aging/neurodegenerative disorders may contribute to its reduction.
Long-term depression- LTD involves the weakening of synapses which aren’t used. This may account for memory loss symptoms of neurodegenerative disorders such as Alzheimer’s.
So where do we actually see neuroplasticity? Adaptive neuroplasticity is instrumental to our daily lives and learning. For example, MRI studies show that level motor dexterity is inversely associated with a decrease in cortical thickness in the hand regions of the cortices (an example of structural brain plasticity). This decrease in thickness may be due to the synaptic pruning discussed earlier. Conversely, enhanced phonological processing is associated with a thicker left inferior frontal cortex. Brain plasticity has also been documented in visually impaired individuals, where the individuals’ brains rewire to improve other senses, such as hearing and smell. Maladaptive neuroplasticity has not been as well researched. Declining neuroplasticity with time is known to contribute to greater difficulty in learning new tasks as we age. In addition, one study proposed that the maladaptive behavior of drug addicts may be a result of drug-induced changes in prefrontal neuronal structure. Similarly, it is known that cognitive and motor functions in adulthood are negatively impacted by the reduced complexity of prefrontal cortex neurons due to prenatal stress. In more recent years, this concept has led researchers to believe that maladaptive neuroplasticity may be a cause of certain neuropsychiatric disorders, or vice versa. Neuroplasticity and Neuropsychiatric Disorders Neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease are associated with neuronal loss in multiple brain regions. The impaired synaptic plasticity in these affected brain regions is thought to be a major contributor to the progressive cognitive and motor deficits seen in patients with dementia. Neuroplasticity has a role in disorders like Post Traumatic Stress Disorder (PTSD) as well. One really interesting study found that veterans with current PTSD symptoms had significantly smaller hippocampal volumes than recovered veterans and veterans who never developed PTSD. These results may allude to the idea of a reversal of hippocampal volume loss after PTSD recovery, or that a smaller hippocampal volume causes greater risk of developing chronic PTSD. This indicates that adaptive structural neuroplasticity is either a result of recovering from PTSD, or maladaptive structural neuroplasticity increases risk of developing PTSD. Similarly, mental illnesses such as Major Depressive Disorder (MDD) or chronic/mood anxiety disorders are thought to cause maladaptive neuroplasticity. In these neuropsychiatric disorders, maladaptive neuroplasticity has the result of persisting symptoms. The relationship between neuroplasticity and neuropsychiatric disorders means that we could use neuroplasticity as a way to promote recovery. Currently, few human studies have been done to demonstrate the effect of certain medications on brain plasticity and therefore healing. However, the possibilities are truly endless. Many studies have found that successful medication treatment reverses hippocampal volume loss in patients with PTSD and depression. Furthermore, as synaptogenesis is stimulated by exposure to new experiences, induced brain stimulation has been theorized to increase grey matter volume, a change which is characteristic of antidepressant response. Moreover, the effect of deep brain stimulation on brain structure and connectivity has been used to effectively treat a few symptoms of Parkinson’s Disease in some cases. Simply exercising more has also been found to increase hippocampal neuroplasticity in animal studies, and by extension, can be looked at as a possible supplementary treatment for neuropsychiatric conditions. Exercise has already been associated with reduced symptoms of MDD and reduced cognitive deficits in MDD, schizophrenia, and Alzheimer’s disease. In conclusion, neuroplasticity is critical in our daily learning and memory processes, but can result in reduced brain health if it is maladaptive. Further studies should be done to understand the extent of neuroplasticity’s role on the development and persistence of neuropsychiatric disorders. By understanding this relationship, we can better implement adaptive neuroplasticity in the treatments of these disorders, and promote more successful healing.
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