Sport Physiology & Management Investigations

Sport Physiology & Management Investigations

The effect of different training periods on beta-amyloid 42 index in hippocampus of streptozotocin-induced diabetic male rats

Document Type : Original Article

Authors
Mahin Hayati 1
Jafar Zarghoshi 2
Gholamreza Dabirifar 2
Mohamadreza Yousefi 3
Mahnaz Omidi 3
1 Graduated from the Department of Sports Sciences, Ilam Branch, Islamic Azad University, Ilam, Iran
2 MSc in Exercise Physiology, Department of Physical Education and Sport Sciences, Ilam Branch, Islamic Azad University, Ilam, Iran
3 Assistant Professor in Exercise Physiology, Department of Physical Education and Sport Sciences, Ilam Branch, Islamic Azad University, Ilam, Iran
Abstract
The aim of the present study was to investigate the effect of different training periods on beta-amyloid 42 index in the hippocampus of streptozotocin-induced diabetic male rats. For this purpose, 84 male Wistar rats weighing 281± 28 g were randomly divided into 4 groups of 21. Subjects were divided into control, exercise, diabetes, diabetes and exercise groups. Simple variance analysis and repeated measures analysis of variance were used to investigate the changes of beta-amyloid 42. The results of analysis of variance in repeated measures showed that there was a significant difference in beta-amyloid 42 at different stages (8, 4 and 12 weeks of training) (P = 0.001). Multiple Bonferroni comparisons revealed that the levels of beta-amyloid 42 were significantly different during all stages of exercise (4 weeks (P = 0.37), 8 weeks (P = 0.001) and 12 weeks (P = 0.001)).In general, it can be concluded that in all 3 different times (4, 8 and 12 weeks) the amount of beta-amyloid 42 in the control and diabetes groups was higher than the exercise, diabetes and exercise groups, respectively. In diabetes, over time (from 4 weeks to 8 and then 12 weeks) the amount of beta-amyloid 42 increases and continuous aerobic training reduces this variable.
Keywords
Beta Amyloid 42
Continuous Aerobic Exercise
Diabetes Mellitus
Hippocampus

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    1. Anık A, Çatlı G, Abacı A, Böber E. Maturity-onset diabetes of the young (MODY): an update. Journal of pediatric endocrinology and metabolism. 2015;28(3-4):251-63.
    2. Barbagallo M, Dominguez LJ. Type 2 diabetes mellitus and Alzheimer’s disease. World journal of diabetes. 2014;5(6):889.
    3. Infante-Garcia C, Ramos-Rodriguez JJ, Galindo-Gonzalez L, Garcia-Alloza M. Long-term central pathology and cognitive impairment are exacerbated in a mixed model of Alzheimer’s disease and type 2 diabetes. Psychoneuroendocrinology. 2016;65:15-25.
    4. Frisardi V, Solfrizzi V, Seripa D, Capurso C, Santamato A, Sancarlo D, et al. Metabolic-cognitive syndrome: a cross-talk between metabolic syndrome and Alzheimer's disease. Ageing research reviews. 2010;9(4):399-417.
    5. Selkoe DJ. The molecular pathology of Alzheimer's disease. Neuron. 1991;6(4):487-98.
    6. Chen G, Chen KS, Knox J, Inglis J, Bernard A, Martin SJ, et al. A learning deficit related to age and β-amyloid plaques in a mouse model of Alzheimer's disease. Nature. 2000;408(6815):975-9.
    7. Wallenstein GV, Hasselmo ME, Eichenbaum H. The hippocampus as an associator of discontiguous events. Trends in neurosciences. 1998;21(8):317-23.
    8. Gispen WH, Biessels G-J. Cognition and synaptic plasticity in diabetes mellitus. Trends in neurosciences. 2000;23(11):542-9.
    9. Jolivalt CG, Hurford R, Lee CA, Dumaop W, Rockenstein E, Masliah E. Type 1 diabetes exaggerates features of Alzheimer's disease in APP transgenic mice. Experimental neurology. 2010;223(2):422-31.
    10. Plaschke K, Kopitz J, Siegelin M, Schliebs R, Salkovic-Petrisic M, Riederer P, et al. Insulin-resistant brain state after intracerebroventricular streptozotocin injection exacerbates Alzheimer-like changes in Tg2576 AβPP-overexpressing mice. Journal of Alzheimer's disease. 2010;19(2):691-704.
    11. Alafuzoff I, Aho L, Helisalmi S, Mannermaa A, Soininen H. β‐Amyloid deposition in brains of subjects with diabetes. Neuropathology and applied neurobiology. 2009;35(1):60-8.
    12. Mohammadi ZF, Khezri A, Ebrahimzadeh M. The effects of voluntary exercise on a running wheel and allium paradoxum on tau protein in the cerebellum of diabetic rats. Journal of Isfahan Medical School. 2012;30(185).
    13. Pierre W, Gildas AJH, Ulrich MC, Modeste W-N, azTélesphore Benoît N, Albert K. Hypoglycemic and hypolipidemic effects of Bersama engleriana leaves in nicotinamide/streptozotocin-induced type 2 diabetic rats. BMC complementary and alternative medicine. 2012;12(1):264.
    14. Skovso S. Modeling type 2 diabetes in rats using high fat diet and streptozotocin. J Diabet Investig 5 (4): 349–358. 2014.
    15. Kim D-Y, Jung S-Y, Kim T-W, Lee K-S, Kim K. Treadmill exercise decreases incidence of Alzheimer’s disease by suppressing glycogen synthase kinase-3β expression in streptozotocin-induced diabetic rats. Journal of exercise rehabilitation. 2015;11(2):87.
    16. Janson J, Laedtke T, Parisi JE, O’Brien P, Petersen RC, Butler PC. Increased risk of type 2 diabetes in Alzheimer disease. Diabetes. 2004;53(2):474-81.
    17. Planel E, Tatebayashi Y, Miyasaka T, Liu L, Wang L, Herman M, et al. Insulin dysfunction induces in vivo tau hyperphosphorylation through distinct mechanisms. Journal of Neuroscience. 2007;27(50):13635-48.
    18. Moroz N, Tong M, Longato L, Xu H, de la Monte SM. Limited Alzheimer-type neurodegeneration in experimental obesity and type 2 diabetes mellitus. Journal of Alzheimer's disease. 2008;15(1):29-44.
    19. Phiel CJ, Wilson CA, Lee VM-Y, Klein PS. GSK-3α regulates production of Alzheimer's disease amyloid-β peptides. Nature. 2003;423(6938):435-9.
    20. Sun X, Sato S, Murayama O, Murayama M, Park J-M, Yamaguchi H, et al. Lithium inhibits amyloid secretion in COS7 cells transfected with amyloid precursor protein C100. Neuroscience letters. 2002;321(1-2):61-4.
    21. Wang Y, Simar D, Fiatarone Singh MA. Adaptations to exercise training within skeletal muscle in adults with type 2 diabetes or impaired glucose tolerance: a systematic review. Diabetes/metabolism research and reviews. 2009;25(1):13-40.
    22. Yaghoubi A SJM, Falah Mohammadi Z, Hedayati Me, Hajizadeh Moghadam A. The effect of eight weeks of aerobic training on levels of amyloid beta 1and γ-secretase in the hippocampus of Alzheimer's male Koomesh Journal. 2015;17(14).
    23. Law LL, Rol RN, Schultz SA, Dougherty RJ, Edwards DF, Koscik RL, et al. Moderate intensity physical activity associates with CSF biomarkers in a cohort at risk for Alzheimer's disease. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring. 2018;10(1):188-95.
    24. He X-f, Liu D-x, Zhang Q, Liang F-y, Dai G-y, Zeng J-s, et al. Voluntary exercise promotes glymphatic clearance of amyloid beta and reduces the activation of astrocytes and microglia in aged mice. Frontiers in molecular neuroscience. 2017;10:144.
    25. Adlard PA, Perreau VM, Pop V, Cotman CW. Voluntary exercise decreases amyloid load in a transgenic model of Alzheimer's disease. Journal of Neuroscience. 2005;25(17):4217-21.
    26. Giménez-Llort L, García Y, Buccieri K, Revilla S, Sunol C, Cristofol R, et al. Gender-specific neuroimmunoendocrine response to treadmill exercise in 3xTg-AD mice. International Journal of Alzheimer’s Disease. 2010;2010.
    27. Um HS, Kang EB, Cho IH, Kim CH, Cho JS, Hwang DY. The combination of exercise training and α-lipoic acid treatment has therapeutic effects on the pathogenic phenotypes of Alzheimer's disease in NSE/APPsw-transgenic mice. International journal of molecular medicine. 2010;25(3):337-46.
    28. Ke H-C, Huang H-J, Liang K-C, Hsieh-Li HM. Selective improvement of cognitive function in adult and aged APP/PS1 transgenic mice by continuous non-shock treadmill exercise. Brain research. 2011;1403:1-11.
    29. Schmitz A, Schneider A, Kummer MP, Herzog V. Endoplasmic reticulum‐localized amyloid β‐peptide is degraded in the cytosol by two distinct degradation pathways. Traffic. 2004;5(2):89-101.
    30. Turner PR, O’Connor K, Tate WP, Abraham WC. Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory. Progress in neurobiology. 2003;70(1):1-32.
    31. Um HS, Kang EB, Leem YH, Cho IH, Yang CH, Chae KR, et al. Exercise training acts as a therapeutic strategy for reduction of the pathogenic phenotypes for Alzheimer's disease in an NSE/APPsw-transgenic model. International journal of molecular medicine. 2008;22(4):529-39.
    32. Nichol KE, Poon WW, Parachikova AI, Cribbs DH, Glabe CG, Cotman CW. Exercise alters the immune profile in Tg2576 Alzheimer mice toward a response coincident with improved cognitive performance and decreased amyloid. Journal of neuroinflammation. 2008;5(1):1-15.
    33. Butovsky O, Bukshpan S, Kunis G, Jung S, Schwartz M. Microglia can be induced by IFN-γ or IL-4 to express neural or dendritic-like markers. Molecular and Cellular Neuroscience. 2007;35(3):490-500.
    34. de Souto Barreto P, Andrieu S, Payoux P, Demougeot L, Rolland Y, Vellas B, et al. Physical activity and amyloid‐β brain levels in elderly adults with intact cognition and mild cognitive impairment. Journal of the American Geriatrics Society. 2015;63(8):1634-9.
    35. Parachikova A, Nichol K, Cotman C. Short-term exercise in aged Tg2576 mice alters neuroinflammation and improves cognition. Neurobiology of disease. 2008;30(1):121-9.
    36. Yuede CM, Zimmerman SD, Dong H, Kling MJ, Bero AW, Holtzman DM, et al. Effects of voluntary and forced exercise on plaque deposition, hippocampal volume, and behavior in the Tg2576 mouse model of Alzheimer's disease. Neurobiology of disease. 2009;35(3):426-32.