APOEε4 impacts up-regulation of brain-derived neurotrophic factor after a six-month stretch and aerobic exercise intervention in mild cognitively impaired elderly African Americans: A pilot study

被引:46
作者
Allard, Joanne S. [1 ]
Ntekim, Oyonumo [2 ]
Johnson, Steven P. [3 ]
Ngwa, Julius S. [4 ]
Bond, Vernon [3 ]
Pinder, Dynell [1 ]
Gillum, Richard F. [4 ]
Fungwe, Thomas V. [2 ]
Kwagyan, John [5 ]
Obisesan, Thomas O. [3 ]
机构
[1] Howard Univ, Coll Med, Dept Physiol & Biophys, Washington, DC 20059 USA
[2] Howard Univ, Dept Nutr Sci, Sch Nursing & Allied Hlth Sci, Washington, DC 20059 USA
[3] Howard Univ Hosp, Dept Med, Div Geriatr, 2041 Georgia Ave NW, Washington, DC 20060 USA
[4] Howard Univ Hosp, Dept Internal Med, Washington, DC USA
[5] Howard Univ Hosp, Dept Community & Family Med, Washington, DC USA
关键词
Aerobic exercise; BDNF; APOE; Oxygen consumption; African Americans; Mild cognitive impairment; FACTOR MESSENGER-RNA; ALZHEIMERS-DISEASE; BDNF LEVELS; APOLIPOPROTEIN-E; SERUM BDNF; PARKINSONS-DISEASE; VOLUNTARY EXERCISE; PHYSICAL-FITNESS; DEMENTIA; AGE;
D O I
10.1016/j.exger.2016.11.001
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Possession of the Apolipoprotein E (APOE) gene 84 allele is the most prevalent genetic risk factor for late onset Alzheimer's disease (AI)). Recent evidence suggests that APOE genotype differentially affects the expression of brain-derived neurotrophic factor (BDNF). Notably, aerobic exercise-induced upregulation of BDNF is well documented; and exercise has been shown to improve cognitive function. As BDNF is known for its role in neuroplasticity and survival, its upregulation is a proposed mechanism for the neuroprotective effects of physical exercise. In this pilot study designed to analyze exercise-induced BDNF upregulation in an understudied population, we examined the effects of APOE epsilon 4 (84) carrier status on changes in BDNF expression after a standardized exercise program. African Americans, age 55 years and older, diagnosed with mild cognitive impairment participated in a six-month, supervised program of either stretch (control treatment) or aerobic (experimental treatment) exercise. An exercise-induced increase in VO(2)Max was detected only in male participants. BDNF levels in serum were measured using ELISA. Age, screening MMSE scores and baseline measures of BMI, VO(2)Max, and BDNF did not differ between epsilon 4 carriers and non-epsilon 4 carriers. A significant association between epsilon 4 status and serum BDNF levels was detected. Non-epsilon 4 carriers showed a significant increase in BDNF levels at the 6 month time point while epsilon 4 carriers did not. We believe we have identified a relationship between the epsilon 4 allele and BDNF response to physiologic adaptation which likely impacts the extent of neuroprotective benefit gained from engagement in physical exercise. Replication of our results with inclusion of diverse racial cohorts, and a no-exercise control group will be necessary to determine the scope of this association in the general population. (C) 2016 The Authors. Published by Elsevier Inc.
引用
收藏
页码:129 / 136
页数:8
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