Robert Hogan explores neuroplasticity.
Have you ever thought about the underlying causes of brain diseases, such as Alzheimer’s? Maybe so, maybe not, either way, I’m here to break down some of the details of one of the brain’s most powerful features - neuroplasticity, also referred to as synaptic plasticity. This article is going to keep it relatively light, focussing on its positive effects in regeneration, in stroke patients, for example, as well as examining its role in diseases like Alzheimer’s. Neuroplasticity is directly involved in some of the brain’s most critical functions, however, its ability decreases drastically with age, resulting in diseases of the brain.
Before we get to the interesting parts, I’ll bore you with the actual science behind neuroplasticity. Fundamentally, it is the ability for the human brain to form new synaptic connections in response to environmental changes, learning, or injury. In less scientific jargon, this is the brain’s capability to connect different parts of the brain together through junctions, which can result in different brain functions, such as learning or memory. At a younger age, the brain is said to be ‘more plastic’, making it more open to forming these new connections. As the brain ages, this plasticity decreases quite drastically, making us more susceptible to brain damage, culminating in brain diseases such as Alzheimer’s Disease.
Neuroplasticity is quite a complex process, as is the case with many aspects of neural function. At its simplest, it involves the alteration of synaptic pathways. Getting a little more specific, these pathways can either be strengthened or weakened depending on the frequency of their usage. In other words, synapses that are used more frequently become strengthened and those used less frequently can be weakened. Sounds simple, right? Well, it becomes a little more complicated when you throw in the more official terminology, stating that Long Term Potentiation strengthens synapses as a result of high-frequency stimulation, and Long Term Depression weakens synapses as a result of low-frequency stimulation. Maybe we’ll stick to less scientific language.
I previously mentioned that neuroplasticity decreases with age, this is the case for a number of reasons. There is a molecular shift, pushing for increased Long Term Depression, leading to the weakening of synaptic connections. The structure of the brain as well as the supply of blood flow are negatively impacted by aging. In the case of Alzheimer’s Disease, there are increased levels of damaging proteins in the brain, damaging the molecular environment of various parts of the brain, directly decreasing the effects of neuroplasticity, preventing the brain from strengthening synapses, directly impacting memory formation and retention. Alzheimer’s is said to be a ‘neurodegenerative’ disease - this is a complicated way of saying it occurs as a result of failure within some part of the brain.
Discussions surrounding neuroplasticity typically focus on the aforementioned negative connotations of decreased function, but I’d like to draw focus to its importance as we age. Stroke patients are prime examples of the extraordinary capabilities of neuroplasticity. Following the occurrence of a stroke, the brain begins to form new neural connections, assigning function to areas that haven’t been damaged by the stroke, and ultimately facilitate recovery from the stroke. Without this profound ability, any damage inflicted on the brain would be irreversible.
I’ll leave it there to avoid getting overly complex, but there’s a number of scientific articles that will go into the finer details of this remarkable concept and truly incredible ability of the brain. Neuroplasticity is a fundamental trait of the nervous system of a vast array of species, but its ability in humans is critical to our normal brain function, as well as recovery from disease, and its decreased ability in older age plays a significant role in disease progression, illuminating its importance.