بررسی مکانیسم عصب شناسی ورزش در دوران سالمندی: مرور روایتی

Extended Abstract

Introduction: The global senior population is rising; by 2030, one in six individuals will be 60 years or older, as reported by the World Health Organization (WHO). This tendency has resulted in heightened focus in scientific study around aging and the quality of life for the elderly. Advanced age is acknowledged as the primary risk factor for the majority of neurological disorders, including Alzheimer's and Parkinson's diseases, particularly among the senior population. Consequently, elderly individuals ought to implement preventive measures and adhere to a healthful lifestyle. Multiple risk factors, including as smoking, physical inactivity, obesity, and hypertension, may facilitate the onset of dementia and associated disorders. Aging induces alterations in the brain, characterized by reduced brain volume, diminished cortical density, decreased white matter, lowered metabolic activity and mitochondrial function, as well as modifications in neurotransmitter levels. The aging process modifies learning and memory due to a reduction in brain capacity, accompanied by the atrophy and alteration of the frontal lobe and hippocampus. The cerebral cortex's thickness diminishes with age, potentially resulting in a reduction in information processing speed. The reduction of neurotransmitters including dopamine, serotonin, and norepinephrine in advanced age impacts mood, memory, and cognitive abilities. The human brain necessitates a substantial amount of metabolic energy for optimal functioning. Notwithstanding its diminutive size, the brain utilizes approximately 20% of the body's overall oxygen supply. Due to their restricted glycolytic capability, neurons are significantly reliant on mitochondrial energy synthesis. Approximately 90% of adenosine triphosphate (ATP) synthesis in the brain transpires within mitochondria. This energy is crucial for various cellular functions, including the synthesis, secretion, and recycling of neurotransmitters, as well as the maintenance of neuronal membrane potential. In addition to energy metabolism, mitochondria are crucial for mechanisms associated with cell survival and death, including the maintenance of cellular oxidative equilibrium, the regulation of apoptotic pathways, and the facilitation of synaptic plasticity. Mitochondria participate in intracellular calcium homeostasis. For instance, mitochondria in synaptic terminals regulate intracellular calcium levels by storing or releasing excess amounts. Mitochondrial malfunction in synaptic mitochondria disrupts neurotransmission, resulting in cellular alterations that can vary from slight modifications in neuronal function to neuronal death and degeneration. Mitochondria are significant generators of reactive oxygen species (ROS) and are also susceptible to ROS-induced toxicity. Epidemiological studies indicate a substantial correlation between physical activity and a diminished risk of Alzheimer’s disease and dementia. Engagement in physical activity correlates with a substantial risk decrease of 45% for Alzheimer's disease and 28% for dementia. This illustrates the capacity of lifestyle modifications, especially physical activity, to enhance neuroprotection. Evidence unequivocally demonstrates that exercise confers numerous advantages for cerebral health and functionality. Until recently, it was believed that the adult brain lacked regenerative capabilities; however, ongoing discussions persist. Notably, the hippocampus, a critical region for learning and memory and particularly susceptible to Alzheimer’s disease, continues to produce new neurons in adults into their 90s. Exercise is one of the rare stimuli capable of inducing neurogenesis in the adult brain. Exercise stimulates neurogenesis, enhances hippocampus volume and blood flow, and augments memory in both mice and humans. Even minimal-intensity exercise, such as walking, enhances hippocampus activity linked to memory enhancement in healthy individuals. Exercise also mitigates the pace of cognitive decline over time in both healthy persons and those with various neurological diseases. Likewise, physical activity diminishes the incidence of dementia and can impede its advancement. The noted health advantages are partially ascribed to exercise's influence on the expression or augmentation of neurotrophins, essential chemicals that enhance neuronal architecture in the brain. Elevated concentrations of neurotrophins, especially brain-derived neurotrophic factor (BDNF), are associated with enhanced neuronal architecture. Brain-derived neurotrophic factor (BDNF) is a protein belonging to the neurotrophin family, located in the brain and peripheral organs, such as skeletal muscle. Neurons within the central nervous system are the primary makers of BDNF, which is essential for memory and learning functions. It interacts with the tyrosine kinase B (TrkB) receptor and facilitates processes like neurogenesis, axonal development, and synaptogenesis. Scientific data indicates that the brain is the primary generator of this component in circulation both at rest and during exercise, with its localized effects within the brain. It also affects physiological systems including glucose metabolism and lipid oxidation. Research indicates that endurance exercise enhances BDNF expression, leading to an increase in dendritic spine density and dendritic branching. These structural alterations have been associated with beneficial enhancements in memory and learning.

Conclusion: Regular exercise in old age is known to be an effective factor in maintaining and promoting brain health. Extensive studies have shown that regular physical activity can improve cognitive functions such as memory, attention, and information processing speed. These improvements are especially significant in older adults who are at risk of cognitive decline or dementia. From a neurological mechanism perspective, exercise increases the brain's neuroplasticity; that is, the brain's ability to create and rebuild new neural connections, which is the basis for learning and memory.

Footnotes

Funding: This article has not received any grants.

Authors’ contribution: F.R. participated in the design of the study and manuscript writing.

Conflict of interest: There is no conflict of interest.