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KMID : 0613820080180060796
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Journal of Life Science
2008 Volume.18 No. 6 p.796 ~ p.803
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The Effect of Exercise Training on Aβ-42, BDNF, GLUT-1 and HSP-70 Proteins in a NSE/ APPsw-transgenic Model for Alzheimer’s Disease
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Eum Hyun-Sub
Kang Eun-Bum
Lim Yea-Hyun
Lee Jong-Rok
Cho In-Ho
Kim Young-Soo
Chae Kab-Ryoung
Hwang Dae-Yean
Kwak Yi-Sub
Oh Yoo-Sung
Cho Joon-Yong
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Abstract
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Mutations in the APP gene lead to enhanced cleavage by β- and γ-secretase, and increased Aβ formation, which are closely associated with Alzheimer’s disease (AD)-like neuropathological changes. Recent studies have shown that exercise training can ameliorate pathogenic phenotypes (Aβ-42, BDNF, GLUT-1 and HSP70) in experimental models of Alzheimer’s disease. Here, we have used NSE/APPsw transgenic mice to investigate directly whether exercise training ameliorates pathogenic phenotypes within Alzheimer’s brains. Sixteen weeks of exercise training resulted in a reduction of Aβ-42 peptides and also facilitated improvement of cognitive function. Furthermore, GLUT -1 and BDNF proteins produced by exercise training may protect brain neurons by inducing the concomitant expression of genes that encode proteins (HSP-70) which suppress stress induced neuron cell damages from APPsw transgenic mice. Thus, the improved cognitive function by exercise training may be mechanistically linked to a reduction of Aβ-42 peptides, possibly via activation of BDNF, GLUT-1, and HSP-70 proteins. On the basis of the evidences presented in this study, exercise training may represent a practical therapeutic management strategy for human subjects suffering from Alzheimer’s disease.
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KEYWORD
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Alzheimer’sdisease(AD), amyloidβ-42(Aβ-42), heatshockprotein-70(HSP-70), glucosetransporter-1(GLUT-1), brainderivedneurotropicfactor(BDNF), enduranceexercisetraining
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