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found a significant decrease in activation intensity of eleven brain regions by fMRI after a 12-week supervised treadmill walking, which suggests exercise intervention enhances neural efficiency. confirmed that exercise-related cognitive benefits point to cerebral blood flow (CBF) and cerebrovascular regulation Smith et al.

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A six-month randomized trial using resistance training and aerobic training finds functional changes in three regions of cortex and hemodynamic activity in the lingual gyrus Guiney et al. The mechanisms of exercise for improving cognition appear to be complex and unclear, including increased blood volume and capillarization, decreased reactive oxygen species (ROS) and oxidative stress, reduced A β load and the levels of hyperphosphorylated tau proteins, the modulation of cholinergic system, and the regulation of expression of brain-derived neurotrophic factor.

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On the other hand, a growing base of evidence has indicated that exercise interventions enhance neuroplasticity, improve cognitive function and the ability of daily life, and reduce rates of neuropsychiatric symptoms. Drug treatment is always a challenge because of its great cost obviously. However, there has been no definite evidence in favor of the appropriate duration and the progression of disease when drug discontinuance. Cholinesterase inhibitors (donepezil, galantamine, and rivastigmine), memantine, and vitamin E have shown at least some efficacy in cognitive and functional decline. Pharmacological and exercise therapies are the major intervention targets of AD. Currently, AD is diagnosed through insoluble amyloid β-peptide (A β) in extracellular plaques and agminated tau protein in the intracellular neurofibrillary tangles by the detection of postmortem. Alzheimer's disease is becoming the fifth leading cause of death in people older than 65 years, and there will be 115 million people worldwide who will suffer from AD by 2050. Alzheimer's disease (AD) and other dementias have a huge impact on the people with the disease, and taking care of them is a huge task for their families. Older adults complain of subjective gradual cognitive decline, and some of them are likely to develop dementia without efficient intervention. Therefore, taking exercise intervention in the early stage of MCI and healthy aging at the risk of AD could slow down the process of cognitive impairment and provide a promising cost-effective nonpharmacological therapy to dementia.ĭemographic changes make dementia an intractable social problem, and strategies for maintaining cognitive function with the growth of the age are seriously needed. MCI is the preclinical stage of AD in which neurodegeneration may be reversed via neuroplasticity. On the other hand, accumulating evidence suggests that exercise intervention may ameliorate the progression of cognitive impairment in aging ones while the standard strategy is lacking based on different levels of cognitive decline especially in mild cognitive impairment (MCI) and AD. However, in most cases, drug therapy is accompanied with clinical delays when older adults have suffered from cognitive decline in episodic memory, working memory, and executive function. Pharmacotherapy has always been in a dominant position for the treatment of AD. Alzheimer's disease (AD) is a progressive neurodegenerative disease with the syndrome of cognitive and functional decline.












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