Brain plasticity refers to the extraordinary ability of the brain to modify its own structure and function following changes within the body or in the external environment. This adaptability is strongest in childhood (explaining the fast learning abilities of children) but remains a fundamental and significant lifelong property of the brain (Society for Neurosciences, 2012). The idea of brain plasticity opposes the previously believed ‘Critical Period Concept’, which states that development occurs within a time frame with a definitive beginning and end, after which development cannot ensue as easily (Colombo, 1982). This paper will discuss the understanding and nature of brain plasticity in the following five conditions that can affect the aging human; Alzheimer’s disease, Parkinson’s disease, Depression, recovery after stroke and recovery after brain injury.
Alzheimer’s Disease
It is noted that age related diseases such as Alzheimer’s can have a detrimental effect on ageing individuals and their carers. Although pharmaceuticals have been widely used to treat the lesions, they often lack the ability to fully cure or prevent the disease. As a result, researchers are developing alternative approaches to treatment such as physical exercise (Erikson, Weinstein and Lopez, 2012). Longitudinal neuroimaging studies have highlighted that individuals participating in high levels of exercise, possessed a larger hippocampal and prefrontal brain area which corresponds to fewer memory impairments. Research such as this supports the idea that physical exercise is beneficial to Alzheimer’s Disease sufferers, and has led to the encouragement of exercise therapy in addition to pharmaceuticals. This is supported by Erickson, Gildengers and Butters (2013). It is suggested that exercise has the capability of enhancing natural plasticity to improve emotional and cognitive functioning in later life.
Parkinson’s Disease
Exercise was often discouraged for Parkinson’s disease sufferers, since it was suggested that the pathology may be negatively affected. However, recent studies have since emerged showing that exercise may progress neuroprotection and restoration which could result in slowing, and potentially halting disease progression (Hirsch and Farley, 2009). Animal studies (Fisher et al, 2004) have shown that treadmill exercise has the capability of reducing lesions in mice injected with methyl, phenyl, tetrahydropyridine (MPTP). Although the exercise performed by the mice in this investigation would not be sufficient to reduce lesions in the human brain, the study does illustrate that exercise has a positive effect in assisting the recovery of Parkinson’s Disease. This shows that the brain is capable of plasticity in later life as neuroprotection and restoration is feasible if the sufferer partakes in physical exercise as part of their treatment.
Depression
Anti-depressants have been shown to reactivate plasticity in an adult cortex, similar to that of an infant. This plasticity is shown to be particularly beneficial when combined with psychotherapy and this results in a more successful recovery (Castren, 2013). This is shown in the work of Vetencourt, Sale and Viegi et al (2008), where rats were given long-term fluoxetine treatment. It was found that the rats’ developed visual cortex was reorganised, suggesting that the same effect is possible in the human visual cortex. It is proposed that the effect of the antidepressants could assist in the treatment of the depression, even in later life when the plasticity of the brain is supposedly worsened.
Cooney and Dwan et al (2013) discuss that antidepressants can have negative side effects and that physical exercise is an alternative therapy offered to sufferers by physicians. It is proposed that nerve cell growth and protection can be stimulated by exercise and that this plasticity can improve the patients’ mental state.
As a result of the research into the benefits of physical exercise on conditions such as those mentioned above, the ‘Exercise is Medicine’ programme has been launched by the American Medical Association. This programme is designed to educate medical professionals on the importance of exercise in mental health and to encourage it to patients.
Recovery after Stroke
It has been suggested that plasticity of our neuronal connections can be influenced by our experiences. Johansson (2000) showed that the brain is capable of compensating for lesions after a stroke providing neuro-imagery, illustrating patterns in the contralateral hemisphere had been altered. In a comparison of post-mortems, healthy 80 year olds were found to have longer dendritic trees than 51 year olds. This dendrite growth illustrates the plasticity of the brain in later life and shows that the brain is developing even in old age.
It has been previously noted that old age can lead to a higher impairment to stroke, however only recently have the underlying causes been made evident (Popa-Wagner et al, 2007). This was shown in an animal study, were older rats suffered a higher impairment than younger rats and were less capable of recovery. This was shown through imaging, in the glial response scar, as the establishment of the scar on the older rats was much higher and recovery was much slower. This is thought to be caused by lower levels of regeneration mechanism activation in later life. It is suggested that this is the cause for elderly sufferers to be less capable of recovery after a stroke than younger individuals.
Recovery after Brain Injury
Similar to the beliefs concerning old age associating to the inhibited recovery after stroke, poorer recovery after traumatic brain injury is also correlated to higher age (Chantal et al, 2003). The relationship between age and outcome of older participants (majority of whom were above the age of 65) was studied and compared against younger participants from meta-analysis. It was found that the likelihood of a poorer recovery is increased by 10% every 10 years of age, concluding that old age has a negative effect on recovery after traumatic brain injury. This poorer recovery rate shows that changes have occurred in the brain since young age and that plasticity is ongoing.
Furthermore, studies are beginning to show that structural changes occur in the cerebral cortex after injury. (Nudo, 2003). It was found that after monkeys with lesions in the primary somatosensory cortex were able to gradually be trained to redevelop sensorimotor skill. The plasticity in the brain after injury suggests to medical professionals that it is possible for brain injury sufferers to reacquire skills after damage has occurred, if the right training is conducted.
In conclusion, it is shown that the brain has the capabilities to modify and restore its structures, even in the ageing human. This is shown by how the brain is able to recover from brain traumas such as dementia, depression and brain injury. This relatively new discovery is able to impact the lives of patients with these conditions positively. The evidence showing that physical exercise can assist pharmaceuticals, has heavily encouraged physicians to recommend physical training programmes to improve recovery rates. It is essential that more research is conducted on brain plasticity, as the potential extent of change achievable in the brain has not yet been determined.