Unlocking Your Superpower: Neuroplasticity

Joannabelle Freya Widjaja
Apr 28
6 min read

Familiarization 101
The Inside Scoop: Growing Connections
Can a Lifestyle Save Lives?
Types
Sources & Works Cited

Familiarization 101

Neuroplasticity, also known as neural or brain plasticity, is the brain's adaptive structural and functional changes in response to intrinsic or extrinsic stimuli. It involves the nervous system reorganizing its structure, functions, or connections, forming and adapting a vast network of neural connections.

The brain is composed of billions of neurons that collect, process, and send information, as well as a complex network of electrical circuits that allow these neurons to communicate with one another. These connections are crucial, as neurons in the brain can send messages to other parts of the body through the nervous system. Younger individuals have an abundance of young neurons, which helps them take in new information quickly and form new neural connections. This greater plasticity is why kids have a much easier time learning a new language than adults.

The brain's cellular or neural networks can undergo rapid change or reconfiguration in a variety of ways and under a wide range of conditions. Rapid branching and synaptic formation of neurons in the developing brain is known as developmental plasticity. Certain synapses become stronger and others weaker as the brain starts processing sensory data. Eventually, some unused synapses are eliminated completely, a process known as synaptic pruning, leaving behind efficient networks of neural connections. Neuroplasticity can be broken down into two major mechanisms: neuronal regeneration/collateral sprouting (synaptic plasticity and neurogenesis) and functional reorganization (equipotentiality, vicariation, and diaschisis). [1][2][3]

The Inside Scoop: Growing Connections

Synaptic plasticity is the ability to make experience-dependent long-lasting changes in the strength of neuronal connections, which can be positively influenced by various factors such as exercise, the environment, repetition of tasks, motivation, neuromodulators, and pharmaceuticals. Aging and neurodegenerative diseases have been associated with a decrease of neuromodulators, which may contribute to a reduction in the ability of synaptic plasticity. The theory of synaptic plasticity has expanded to include more of the evolving complexity of synaptic communication, including spike-timing-dependent plasticity (STDP), metaplasticity, and homeostatic plasticity.

The concept that the brain keeps producing new neurons is known as adult neurogenesis. Josef Altman found evidence of neurogenesis in adult rats, but it has not been convincingly demonstrated in humans. Two locations for adult neurogenesis in humans have been put forward: the olfactory bulb and the hippocampus. The concept that humans undergo adult neurogenesis has been supported by research employing certain biomarkers linked to growing neurons. However, the evidence is complicated as they have also been found in immature neurons, cells that can be found in the human brain that are not newborn nor migrating cells. In order to clarify their function in the brain's plasticity, more precise biomarkers that can distinguish between immature and newborn neurons will probably need to be created.

Functional reorganization is another concept that has been explored. The notion of equipotentiality states that if one side of the brain is injured, the other half can continue to operate normally. This concept morphed into equipotentiality, meaning that if the damage occurred very early, then the brain has the potential to overtake lost functions. Vicariation is the thought that the brain can reorganize other portions of the brain to overtake functions that they were not intended to.

According to the idea of diaschisis, injury to one area of the brain may result in a loss of function in another because of another associated path. Constantin von Monakow proposed this concept to explain why some people lost specific functions (such as speech) but did not have a lesion in the area thought to supply that function. The hypoperfusion of the ipsilateral thalamus following an acute middle cerebral artery (MCA) stroke serves as a demonstration of this.

The theory of diaschisis has evolved over time and is now used to explain a variety of ideas on the brain's functional connections and what happens when damage is done. These concepts include diaschisis 'at rest', functional diaschisis, dynamic diaschisis, connectional diaschisis, and connectome diaschisis. The idea and function of diaschisis will continue to develop and shift as our understanding of the brain's functional connections improves. [1]

Can a Lifestyle Save Lives?

Neuroplasticity operates in various situations, such as natural adult neurogenesis during stroke recovery and stem cell research, which could lead to an enhancement of neurogenesis in adults suffering from stroke, Alzheimer disease, Parkinson disease, or depression. Research suggests that Alzheimer disease in particular is associated with a marked decline in neurogenesis.

Sleep may reduce the likelihood of dementia and Alzheimer's disease by aiding the brain in eliminating poisons like the amyloid protein. Sleep deprivation might increase the risk of dementia and Alzheimer's. Brain health is also influenced by lifestyle choices like exercise, stress reduction, alcohol use, quitting smoking, and preserving a robust social network. The brain can adjust to alterations caused by brain illnesses by developing cognitive reserve through moderately demanding activities like studying, playing an instrument, or reading. Neural networks in people who learn more often are typically better able to handle brain illnesses. [3]

Types

There are four types of neuroplasticity: homologous area adaptation, compensatory masquerade, cross-modal reassignment, and map expansion. When neurons grow too quickly and make too many connections during the first few years of life, a process known as developmental plasticity takes place. Each cerebral cortex cell contains over 2,500 synapses at birth, which is almost twice as many as the typical adult brain by the time the child is two or three years old. Reinforced connections get stronger while unreinforced ones are weaker. Through contact with its environment, these linkages are refined over the course of an organism's existence. For the nervous system to grow properly in early life, certain sensory inputs are necessary. Following this time, fewer connections are maintained, and those that are reinforced by suitable sensory experiences. There are four other forms of neuroplasticity, though.

During early development, homologous area adaptation takes place, allowing brain modules to move their usual functions to regions outside of the damaged module. Because of this feature, the module's stored functions may be replaced with new ones. For instance, the left parietal lobe takes up visuospatial activities at the expense of compromised mathematical abilities if the right parietal lobe is injured early in life. Since children learn to traverse physical space before learning mathematics, timing is also important in this process.

Simply put, compensatory masquerade, the second sort of neuroplasticity, is the brain's ability to come up with another way to complete a job when the first one is unable to follow because of disability. When someone tries to find their way from one place to another, for instance. The majority of people use their innate sense of distance and direction to navigate to varying degrees. A person with a brain injury that impairs their spatial sense, however, will turn to an other method of navigating space, such learning landmarks. Reorganization of preexisting neural networks is the sole alteration that takes place in the brain.

A kind of neuroplasticity known as cross-modal reassignment occurs when new inputs are given to a part of the brain that has been deprived of its primary inputs. For instance, the visual cortex in the occipital lobe, V1, may receive touch input from a blind adult. Touch-oriented trials do not cause V1 activation in sighted individuals. This is due to the fact that neurons, independent of sensory modality, communicate using the same abstract language of electrochemical impulses. Blind people's visual cortices are still capable of cognitive processes, but they rely on touch input to create these representations. This is a shift in a local brain region's functional assignment rather than merely a compensatory mechanism.

One other aspect of neuroplasticity is map expansion, which refers to the adaptability of brain areas that are used for information storage or specialized tasks. In the cerebral cortex, these areas are arranged like a map. This area of the cortical map expands and contracts when a person exercises a function that they execute often. When acquiring and honing a talent, like playing an instrument, this phenomena takes place. As the talent is honed via repeated practice, the area maintains its original expansion. In phantom limb syndrome, where the mouth brain map replaces the arm and hand brain maps, map enlargement has been connected to discomfort. [2]