Traditionally, it was thought that the neurology of normal aging was characterized by significant cell loss and dendrite information is protected degradation. However, when stereological concepts were applied to flow cytometry methodologies, it was shown that considerable cell loss does not happen throughout normal aging and that alterations in dendritic intricacy are minor and geographical area. Even in the absence of sickness, humans and other animals undergo cognitive deterioration as they age. Although diseases are a common cause of behavioral changes in old age, scientists are interested in how to restore brain plasticity to a person in old age. This paper was written with the aim of studying brain plasticity in the elderly.
Researchers and the general public recognize that their cognitive abilities decline with age. For many older persons, the deterioration is becoming so severe that they can no longer live freely and control their lives. While there is some neural deterioration that occurs with age, the brain has the capacity to increase neural activity and develop neural scaffolding to regulate cognitive function. A rise in neuronal volume as a result of mental training or experience is a clear sign of change. However, changes in activation in response to cognitive activity may be indicative of approach modification rather than brain plasticity. The impact of mental training is remarkably long-lasting, although evidence that training benefits transfer to other aspects of cognition is scant.
It was considered that neuroplasticity peaked at a young age and then steadily declined with age. Significant evidence suggesting lifelong brain plasticity has been established in recent years due to enormous breakthroughs in medical imaging tools for assessing brain anatomy and function (Fernandes et al., 2017). Practice allows for improved and refined effectiveness on neurological or other tasks. This dynamic behavioral activity is coupled with changing brain activity, which occurs similarly in young and elderly individuals. In addition to causing functional brain changes, a practice also causes structural changes, such as improvements in specific brain regions and grey and white matter areas that are commonly activated throughout task completion.
The preservation of long-term recollection and plasticity needs the expression of genes; thus, it is not unexpected that these processes change in old animals. Variations in the oscillations of neuronal assemblages that occur with age lead to cognitive decline. Electrophysiological measurements from numerous neurons in the hippocampus of young and old rats, in particular, have shown age variations in the movements of place cells, which correspond with spatial cognition deficiencies (Mateos-Aparicio and Rodríguez-Moreno, 2019). Considering that the typical length is growing across the world, studying the brain processes that cause age-related mental loss is becoming increasingly relevant.
People are living in a very dynamic world where significant technological advances are adopted at a quick speed. This compels folks to forsake old habits in favor of new ones, putting their brains’ agility and flexibility to the test. Based on demographic changes in society, which is described by a continually growing number of older adults, substantiated lifetime neural plasticity provides a solid basis for older adults to maintain their role in society as well as to secure prolonged fully functioning independence and quality of life. A community must provide an environment in which older persons are pushed and encouraged to adapt to new situations, therefore reducing or even reversing the negative consequences of age-related brain deterioration and promoting healthy minds.
References
Fernandes, J., Arida, R. M., & Gomez-Pinilla, F. (2017). Physical exercise as an epigenetic modulator of brain plasticity and cognition. Neuroscience & Biobehavioral Reviews, 80, 443-456.
Mateos-Aparicio, P., & Rodríguez-Moreno, A. (2019). The impact of studying brain plasticity. Frontiers in cellular neuroscience, 13, 66.