Positive Effects of Physical Exercises on Dementia Patients

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Alzheimer’s Disease (AD) and Vascular Cognitive Impairment and Dementia (VCID) are the two most common types of dementia (Cunningham et al., 2015). Dementia also termed Major Neurocognitive Disorder in DSM-5 is an abnormal aging phenomenon and mostly develops later in life. The progressive deterioration of brain functioning is irreversible medical treatments could only slow down the problem. During initial and moderate stages, cognitive symptoms include prospective memory and visuospatial skills impairments, agnosia, as well as difficulties with planning, organization, reasoning, language, sequencing, and abstract information. On the other hand, behavioral symptoms are usually impulsive, including aggression, apathy, agitation, and sundowner syndrome. Patients also experience delusions, changes in mood such as depression and anxiety, different personality, and negative impact on social and occupational functioning. During the late stage, patients’ quality of life is poor. They are unable to move around, communicate, eat, or take care of themselves. Day-to-day activities needed to be entirely supported by family or others. There is also an increased risk of early death due to inactivity and the onset of other illnesses.

Nonetheless, in recent years, the rapid growth of literature suggests that physical exercise, especially aerobic type, is effective in coping with dementia patients’ conditions. The following would discuss and analyze the beneficial effects of physical exercise on dementia patients.

Brain Function

The health of the gray matter and white matter is essential for coping with dementia. The gray matter contains most brain neuron cell bodies, and it is a region responsible for muscle control and sensory perception including vision, hearing, memory, emotions, self-control, speech, and decision making. Studies have found that a group of senior participants recorded larger hippocampal volumes after one year of aerobic exercise, compared with the control group that does only stretching and toning (Ahlskog et al., 2011). In other words, seniors’ brain gray matter volumes could be decreased slower or maintained in size with regular physical exercises.

Except for gray matter, white matter is also damaged in VCID patients which negatively affects information processing (Trigiani & Hamel, 2017). White matter fibers in AD patients also have increased microstructural damage with a strong correlation with low cerebral blood flow. Blood flow in white matter is naturally low and contains less metabolic reserve. Based on research findings, physical exercise enhances the connectivity of white matter (Hayes, Salat, Forman, Sperling, & Verfaellie, 2015). It improves global cerebral blood flow, increases proteins that are responsible for neuronal differentiation and axonal growth, and it also escalates the number of endothelial glucose transporter 1 receptors which deliver glucose to oligodendrocytes where the myelin sheath is produced. Besides, moderate physical exercise increases brain perfusion as research showed there was an improved executive function by using the Stroop test (Lucas et al., 2012). Therefore, physical exercise counteracts the loss of white matter integrity and potentially influences cognition.

Moreover, physical exercise improves the spatial memory of dementia patients by stimulating neuroplasticity mechanisms. Aging rats were used in a study (Vilela et al., 2016). The Aging Wistar rats performed aerobic or strength training for 50 min 3 to 4 days per week and lasts for 8 weeks. After the physical exercise, there was improved cognition in a spatial memory task due to a higher level of synaptic plasticity proteins within the hippocampus. The hippocampus is responsible for memory and progressively degenerates in AD patients. Therefore, physical exercise is crucial for memory improvement in dementia patients.

Furthermore, physical exercise reduces oxidative stress as it is one of the causes of dementia. Studies revealed that there is an inverted U-shape relationship between physical exercise and oxidative stress, which means a moderate amount of physical exercise has an optimized effect (Miyamoto et al., 2013). Physical exercise thus improves mitochondrial function and decreases reactive oxygen species (ROS) production as a neuroprotective mechanism, showing that physical exercise acts as an antioxidant therapy on the brain’s vascular culture.

Lastly, there is toxic protein aggregation accumulation before dementia onset, and it is considered a cause of neuron deterioration process. Physical exercise is proven to significantly reduce levels of amyloid-beta (Aβ) plaque and hyperphosphorylated tau (Trigiani & Hamel, 2017). It is suggested that because of less amyloid, there is less vascular damage induced by the proinflammatory mediators. Besides, the clearance of toxic proteins is also due to improved quality and longer duration of sleep induced by PE. Plus, neuroinflammation is also manifested in dementia. The more toxic protein, the more neuroinflammation. In the early stage of AD, microglia are supposed to slow disease progression since it is responsible for phagocytosing Aβ. However, constant microglial production leads to neuroinflammation which is found in AD patients (Solito, E., & Sastre, M., 2012). Research has shown that physical exercise reduces or even inhibits peripheral inflammation and neuroinflammation. Through the investigation of two groups of Tg2576 AD mouse models, with exercise and no exercise, sedentary mice indicated an increased hippocampal expression of proinflammatory interleukins IL-1β and TNF-α, and reduced levels of interferon-gamma (IFN-γ) and chemokine ligand 3 (Trigiani & Hamel, 2017).

Consequently, physical exercise improves gray and white matter, and spatial memory, and also reduces oxidative stress, toxic protein, and neuroinflammation in dementia patients.

Physical Function

Studies have proven that physical exercise enhances muscle strength, coordination, and endurance, in dementia patients.

Exercise intervention for mild cognitive impairment, and mild to moderate dementia patients are tested and showed significant improvement in balance, mobility, step length, and walking endurance (Lam et al., 2018). For balance, 722 dementia patients were recruited to have exercise intervention and tested with the Berg Balance Scale for six trials. Results showed that patients improved by 3.6 points. Another 242 patients are examined on the functional reach test for six trials, which showed significant improvement by reaching 3.9 centimeters. Participants also performed better in the Tinetti balance assessments after multimodal exercise, Tai Chi, and walking for 20 to 120 minutes at least twice a week. For mobility, 249 moderate-stage dementia patients with multimodal exercises manifested significantly reduced time required to complete the Times Up and Go (TUG) by two sec. Walking speed was also improved by 0.13 m/s in 568 participants with seven trials. For step length, 296 dementia patients showed improved step length by 5 centimeters after adopting multimodal exercise with walking and aerobic workout for 1-2 hours 2 to 3 sessions per week for 15 weeks. For walking endurance, after dementia participants performed multimodal exercises 0.5-1.5 hours 2 to 4 times per week for 9 to 12 months, participants could perform a 6-minute-walk distance of 75 meters.

To sum up, the above studies have proven that physical exercise, especially aerobic and multimodal types, improve physical function in dementia patients including balance, mobility, step length, and walking endurance which are important for day-to-day activities.

Psychological health

As mentioned, dementia patients easily to have changes in mood such as depression and anxiety, especially patients who have good insight and awareness of their condition. On the other hand, physical exercise is beneficial to psychological health.

Physical exercise induces a positive mood in dementia patients. Neurogenesis is stimulated by physical exercise and it helps to reduce anxiety and depression. Physical exercise promotes hippocampal neurogenesis with molecular mechanisms including B-endorphins, angiogenesis, brain-derived neurotrophic factor (BDNF), and serotonin (Ernst, et al., 2006). Firstly, B-endorphins are responsible for coping with stress, pain management, reward feeling, behavioral stability, and maintaining homeostasis. Secondly, angiogenesis refers to the formation of new blood vessels from existing ones. Researchers found that elderly individuals with 3 hours per week of physical exercise for 10 years have more small vessels in the anterior cerebral circulation than the ones who did not have regular exercise. The induced angiogenesis improves peripheral organ blood flow, cerebral blood volume in the motor cortex, and cerebral blood flow (CBF). Improved CBF means improved neurovascular coupling, and it ensures a sufficient supply of oxygen to active neurons, which is dysregulated in AD and VCID. Thirdly, BNDF’s function is to maintain the survival of neurons and synaptic plasticity. However, patients with depression and suicidal thoughts have lower expression of BDNF (Dwivedi Y., 2009). Thereby, an adequate expression of BDNF is needed. Lastly, serotonin regulates mood, sleep, and appetite which is also paramount for patients with depression.

In addition to neurogenesis, physical exercise improves one’s mood by increasing the levels of endocannabinoids which are associated with a sense of well-being, anxiolysis, and analgesia (De Moor, et al. 2006). Physical exercise also promotes the change of the hypothalamic-pituitary-adrenal axis (HPA axis) including more adrenocorticotropic hormone (ACTH) and decreased cortisol production, which induces a positive mood (Wittert, et al, 1996). Finally, self-concept, self-esteem, sense of accomplishment, and social support can be gained through team sports.

As a result, physical exercise not only improves dementia patients’ cognitive and physical function but also generates a positive mood in order to cope with or prevent anxiety and depression caused by the stressful dementia condition.

To recapitulate, dementia is a disease related to brain damage. There are medical treatments for dementia to slow down the progression of deterioration. Some of the drugs target cognitive deficits such as Cholinesterase-inhibitors: Aricept, Exelon, and Reminyl. Some of the drugs target associated symptoms such as SSRIs for depression and anxiety, Antipsychotics for agitation. However, the application of medicine is merely effective for a short-term duration. Instead, physical exercise is a more natural and holistic treatment for dementia patients as it acts as a neuroprotective therapy, physiotherapy, and psychosocial therapy. Dementia cannot be cured, but physical exercise is a successful method to alleviate the condition or even act as dementia prevention for middle-aged people.

Reference

Ahlskog, J. E., Geda, Y. E., Graff-Radford, N. R., & Petersen, R. C. (2011). Physical exercise as a preventive or disease-modifying treatment of dementia and brain aging. Mayo Clinic Proceedings, 86(9), 876–884. https://doi.org/10.4065/mcp.2011.0252
Cunningham, E. L., McGuinness, B., Herron, B., & Passmore, A. P. (2015). Dementia. The Ulster medical journal, 84(2), 79–87.
De Moor, M. H., Beem, A. L., Stubbe, J. H., Boomsma, D. I., & De Geus, E. J. (2006). Regular exercise, anxiety, depression, and personality: a population-based study. Preventive medicine, 42(4), 273–279. https://doi.org/10.1016/j.ypmed.2005.12.002
Dwivedi Y. (2009). Brain-derived neurotrophic factor: role in depression and suicide. Neuropsychiatric disease and treatment, 5, 433–449. https://doi.org/10.2147/ndt.s5700
Ernst, C., Olson, A. K., Pinel, J. P., Lam, R. W., & Christie, B. R. (2006). Antidepressant effects of exercise: evidence for an adult-neurogenesis hypothesis. Journal of psychiatry & neuroscience: JPN, 31(2), 84–92.
Hayes, S. M., Salat, D. H., Forman, D. E., Sperling, R. A., & Verfaellie, M. (2015). Cardiorespiratory fitness is associated with white matter integrity in aging. Annals of Clinical and Translational Neurology, 2(6), 688-698. doi:10.1002/acn3.204
Lam, F. M., Huang, M., Liao, L., Chung, R. C., Kwok, T. C., & Pang, M. Y. (2018). Physical exercise improves strength, balance, mobility, and endurance in people with cognitive impairment and dementia: A systematic review. Journal of Physiotherapy, 64(1), 4-15. doi:10.1016/j.jphys.2017.12.001
Lucas, S. J., Ainslie, P. N., Murrell, C. J., Thomas, K. N., Franz, E. A., & Cotter, J. D. (2012). Effect of age on exercise-induced alterations in cognitive executive function: Relationship to cerebral perfusion. Experimental Gerontology, 47(8), 541-551. doi:10.1016/j.exger.2011.12.002
Miyamoto, N., Maki, T., Pham, L. D., Hayakawa, K., Seo, J. H., Mandeville, E. T., . . . Arai, K. (2013). Oxidative Stress Interferes With White Matter Renewal After Prolonged Cerebral Hypoperfusion in Mice. Stroke, 44(12), 3516-3521. doi:10.1161/strokeaha.113.002813
Solito, E., & Sastre, M. (2012). Microglia function in Alzheimer’s disease. Frontiers in pharmacology, 3, 14. https://doi.org/10.3389/fphar.2012.00014
Trigiani, L. J., & Hamel, E. (2017). An endothelial link between the benefits of physical exercise in dementia. Journal of Cerebral Blood Flow & Metabolism, 37(8), 2649-2664. doi:10.1177/0271678×17714655
Vilela, T. C., Muller, A. P., Damiani, A. P., Macan, T. P., Silva, S. D., Canteiro, P. B., . . . Pinho, R. A. (2016). Strength and Aerobic Exercises Improve Spatial Memory in Aging Rats Through Stimulating Distinct Neuroplasticity Mechanisms. Molecular Neurobiology, 54(10), 7928-7937. doi:10.1007/s12035-016-0272-x
Wittert, G. A., Livesey, J. H., Espiner, E. A., & Donald, R. A. (1996). Adaptation of the hypothalamopituitary adrenal axis to chronic exercise stress in humans. Medicine and science in sports and exercise, 28(8), 1015–1019. https://doi.org/10.1097/00005768-199608000-00011

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Positive Effects of Physical Exercises on Dementia Patients

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