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      Effects of exercise training on stroke risk factors, homocysteine concentration, and cognitive function according the APOE genotype in stroke patients

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          Abstract

          The apolipoprotein E ( APOE) gene has been suggested to be associated with stroke and dementia. However, the effects of exercise training on dementia according to the APOE genotype are not consistent to those reported by previous studies. Therefore, we examined the effects of exercise training on stroke risk factors including blood pressure, lipid profiles, homocysteine (Hcy) concentrations, and cognitive function according to the APOE genotype in stroke patients. We examined the stroke risk factors, Hcy, and cognitive function in 28 ischemic stroke patients before and after 6 months of exercise training. After exercise training, body weight, body mass index (BMI), and percent body fat decreased significantly in both APOE groups. According to the APOE genotype, the changes in BMI in the APOE ɛ4 group higher than those in APOE ɛ3 group significantly. Total cholesterol (TC), low-density lipoprotein (LDL)-C, triglyceride (TG), and Hcy decreased and high-density lipoprotein (HDL)-C increased significantly in the both groups. According to the APOE genotype, systolic blood pressure in the APOE ɛ4 group decreased, but in the APOE ɛ3 group increased after exercise training. TC, LDL-C, and TG in the APOE ɛ4 group decreased more extensively than those in the APOE ɛ3 group after exercise training. VO 2max (maximal oxygen consumption) and cognition increased significantly in both groups. Folate acid intake also increased significantly in both groups. The APOE genotype affects variations in the risk factors of stroke after exercise training. However, the Hcy and cognitive function did not differ based on the APOE genotype.

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          Most cited references43

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          Capitalizing on cortical plasticity: influence of physical activity on cognition and brain function.

          Given the aging populations in many countries throughout the world, there is an increasing interest in lifestyle factors and interventions that will enhance the cognitive vitality of older adults and reduce the risk for age-related neurological disorders, such as Alzheimer's disease. In this review, we evaluate the hypothesis that physical activity and exercise might serve to protect, and also enhance, cognitive and brain function across the adult lifespan. To this end, we critically review three separate literatures that have examined the influence of physical activity and exercise on cognition, brain function and brain structure of adults, including epidemiological or prospective observational studies, randomized human clinical interventions and non-human animal studies. We suggest that this literature supports the claim that physical activity enhances cognitive and brain function, and protects against the development of neurodegenerative diseases. We discuss future directions to address currently unresolved questions, such as interactions between multiple lifestyle factors on offsetting or protecting against cognitive and neural decline, and conclude that physical activity is an inexpensive treatment that could have substantial preventative and restorative properties for cognitive and brain function.
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            Apolipoprotein E polymorphism and cardiovascular disease: a HuGE review.

            This review examines the association between the apolipoprotein (apo) var epsilon gene polymorphism (or its protein product (apo E)), metabolic regulation of cholesterol, and cardiovascular disease. The apo var epsilon gene is located at chromosome 19q13.2. Among the variants of this gene, alleles (*) epsilon2, (*) epsilon3, and (*) epsilon4 constitute the common polymorphism found in most populations. Of these variants, apo (*) epsilon3 is the most frequent (>60%) in all populations studied. The polymorphism has functional effects on lipoprotein metabolism mediated through the hepatic binding, uptake, and catabolism of chylomicrons, chylomicron remnants, very low density lipoprotein (VLDL), and high density lipoprotein subspecies. Apo E is the primary ligand for two receptors, the low density lipoprotein (LDL) receptor (also known as the B/E receptor) found on the liver and other tissues and an apo E-specific receptor found on the liver. The coordinate interaction of these lipoprotein complexes with their receptors forms the basis for the metabolic regulation of cholesterol. Allelic variation in apo var epsilon is consistently associated with plasma concentrations of total cholesterol, LDL cholesterol, and apo B (the major protein of LDL, VLDL, and chylomicrons). Apo var epsilon has been studied in disorders associated with elevated cholesterol levels or lipid derangements (i.e., hyperlipoproteinemia type III, coronary heart disease, strokes, peripheral artery disease, and diabetes mellitus). The apo var epsilon genotype yields poor predictive values when screening for clinically defined atherosclerosis despite positive, but modest associations with plaque and coronary heart disease outcomes. In addition to genotype-phenotype associations with vascular disease, the alleles and isoforms of apo var epsilon have been related to dementias, most commonly Alzheimer's disease.
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              Mechanisms of homocysteine neurotoxicity in neurodegenerative diseases with special reference to dementia.

              Mild to moderate hyperhomocysteinemia is a risk factor for neurodegenerative diseases. Human studies suggest that homocysteine (Hcy) plays a role in brain damage, cognitive and memory decline. Numerous studies in recent years investigated the role of Hcy as a cause of brain damage. Hcy itself or folate and vitamin B12 deficiency can cause disturbed methylation and/or redox potentials, thus promoting calcium influx, amyloid and tau protein accumulation, apoptosis, and neuronal death. The Hcy effect may also be mediated by activating the N-methyl-D-aspartate receptor subtype. Numerous neurotoxic effects of Hcy can be blocked by folate, glutamate receptor antagonists, or various antioxidants. This review describes the most important mechanisms of Hcy neurotoxicity and pharmacological agents known to reverse Hcy effects.
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                Author and article information

                Journal
                J Exerc Rehabil
                J Exerc Rehabil
                Journal of Exercise Rehabilitation
                Korean Society of Exercise Rehabilitation
                2288-176X
                2288-1778
                April 2018
                26 April 2018
                : 14
                : 2
                : 267-274
                Affiliations
                [1 ]Department of Physical Education, Centre for Sport Medicine, Kyung Hee University, Seoul, Korea
                [2 ]Department of Physical Education, College of Education, Dongguk University, Seoul, Korea
                [3 ]Department of Prescription & Rehabilitation of Exercise, College of Physical Exercise, and Department of Kinesiologic Medical Science, Graduate School Dankook University, Cheonan, Korea
                Author notes
                [* ]Corresponding author: Yun-A Shin, https://orcid.org/0000-0002-8480-3454, Department of Prescription & Rehabilitation of Exercise, College of Physical Exercise, and Department of Kinesiologic Medical Science, Graduate School Dankook University, 119 Dandae-ro, Dongnam-gu, Cheonan 31116, Korea, Tel: +82-41-550-3831, Fax: +82-41-550-3831, E-mail: shinagel@ 123456dankook.ac.kr
                Article
                jer-14-2-267
                10.12965/jer.1836108.054
                5931164
                29740562
                8bfd7fad-6019-4432-99a0-c55d071ecfda
                Copyright © 2018 Korean Society of Exercise Rehabilitation

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 27 February 2018
                : 28 March 2018
                Categories
                Original Article

                apoe genotype,homocysteine,cognitive function,exercise training,stroke patients

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