The effect of continuous training with and without caloric restriction on the of tau and amyloid beta gene expressions in aged male rats brain tissue
Subject Areas : Role of Genes in HealthHorieh karimi 1 , Mahtab Moazzami 2 , Ali Yaghoubi 3
1 - Ph.D student of Exercise Physiology, Department of Physical Education and Exercise Science, Bojnourd Branch, Islamic Azad University, Bojnourd, Iran.
2 - Department of Exercise Physiology, Faculty of Sport Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
3 - Department of Physical Education and Exercise Science, Bojnourd Branch, Islamic Azad University, Bojnourd, Iran.
Keywords: Aging, Tau gene, Beta amyloid gene, Continuous exercise, Calorie restriction,
Abstract :
Background and Purpose: Alzheimer's disease, as the most common age-related neurodegenerative disease that Amyloid plaques and interneuron filamentous coils are the two main symptoms of Alzheimer's disease, which are usually associated with amyloid angiopathy in the brain. Materials and methods: 36 old male mice were randomly divided into four control groups, continuous training group and continuous training group with restriction and calorie restriction group according to the entry criteria (same food, homogeneity in terms of age and weight, and same maintenance conditions). Mice participated in 5 sessions (6 weeks, a total of 30 sessions) or 4 sessions per week (8 weeks, a total of 28 sessions) of 60 minutes for eight weeks. Calorie restriction after examining the nutrition of mice for two weeks, between 25 and 30% of the daily calorie consumption of mice is reduced, and calorie restriction is applied in this way. The measurement of blood indices and body composition was done before and after the implementation of the training protocol. Data analysis was performed using the U-Man-Whitney test at a significant level. Results: Our results showed that there is no significant difference between the 4 investigated groups in the expression of tau gene and amyloid beta gene in old male mice with Alzheimer's disease. Conclusion: According to the factors obtained from the study, it seems that continuous training with and without caloric restriction has not been able to change the expression of tau gene and amyloid beta gene in old male rats.
1. Nisbet RM, Polanco JC, Ittner LM, Götz J. Tau aggregation and its interplay with amyloid-β. Acta Neuropathol. 2015;129(2):207-220.
2. Godarzi F, Nikbakht H, Abednatanzi H, Ebrahim K, Ghazalian F. Comparison the effect of aerobic and resistance training on some oxidative parameters and TGF-β in cardiac tissue of elderly rats. RJMS. 2020; 27(3):93-100. [In Persian]
3. Querfurth HW, LaFerla FM. Mechanisms of disease. N Engl J Med. 2010; 362(4): 329-344.
4. Babaei Abraki S, Chavoshi-Nezhad S. Mitochondrial defects and oxidative stress in alzheimer disease. Shefaye Khatam. 2014; 2(1):85-94. [In Persian]
5. Parsa N. Alzheimer’s Disease: A medical challenge of 21st century . J Arak Uni Med Sci. 2011; 14(2):100-108. [In Persian]
6. Akbari Kamrani AA, Shams A, Abdoli B, Shamsipour Dehkordi P. The effect of low and moderate Intensity aerobic exercises on self-concept in older adults. Salmand: Iranian Journal of Ageing. 2015; 10(2):188-195. [In Persian]
7. Peric A, Annaert W. Early etiology of Alzheimer's disease: tipping the balance toward autophagy or endosomal dysfunction?. Acta Neuropathol. 2015;129(3):363-381.
8. Abramov E, Dolev I, Fogel H, Ciccotosto G.D, Ruff E, et al. Amyloid-β as a positive endogenous regulator of release probability at hippocampal synapses. Nature neuroscience. 2009; 12(12):1567-1576.
9. Dorostkar MM, Zou C, Blazquez-Llorca L, Herms J. Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities. Acta Neuropathol. 2015;130(1):1-19.
10. Thal DR, Walter J, Saido TC, Fändrich M. Neuropathology and biochemistry of Aβ and its aggregates in Alzheimer's disease. Acta Neuropathol. 2015;129(2):167-182.
11. Vinters HV. Emerging concepts in Alzheimer's disease. Annu Rev Pathol. 2015;10:291-319.
12. Pasand Mojdeh H, Alipour F, Borhani Haghighi M. Alzheimer's Disease: Background, Current and Future Aspects. Shefaye Khatam. 2016; 4(3):70-80. [In Persian]
13. Biensø RS, Olesen J, Gliemann L, et al. Effects of exercise training on regulation of skeletal muscle glucose metabolism in elderly men. J Gerontol A Biol Sci Med Sci. 2015;70(7):866-872.
14. Lin TW, Shih YH, Chen SJ, et al. Running exercise delays neurodegeneration in amygdala and hippocampus of Alzheimer's disease (APP/PS1) transgenic mice. Neurobiol Learn Mem. 2015;118:189-197.
15. Dao AT, Zagaar MA, Alkadhi KA. Moderate treadmill exercise protects synaptic plasticity of the dentate gyrus and related signaling cascade in a rat model of alzheimer's disease [published correction appears in Mol Neurobiol. 2018 Jan;55(1):901].
16. Salehi A, Abbaszadeh H, Farzanegi P. The Effect of periodic exercise and resveratrol supplementation on the expression of parg coactivator-1 alpha and pyruvate dehydrogenase kinase genes in gastrocnemius muscle of old rats with type 2 diabetes. Intern Med Today. 2019; 26(1):68-81.
17. Khodadadi D, Gharakhanlou R, Nakhdi N, Selimi M, Azimi M, Shahid A. The effect of four weeks prior exercise training on the level of soluble amyloid beta and memory impairment in rats with Alzheimer's disease induced by Aβ-42 injection. Razi Journal of Medical Sciences. 2017; 24(165). [In Persian]
18. Van Dyck CH. Anti-Amyloid-β Monoclonal Antibodies for Alzheimer's Disease: Pitfalls and Promise. Biol Psychiatry. 2018;83(4):311-319.
19. Li HL, Wang HH, Liu SJ, et al. Phosphorylation of tau antagonizes apoptosis by stabilizing beta-catenin, a mechanism involved in Alzheimer's neurodegeneration. Proc Natl Acad Sci U S A. 2007;104(9):3591-3596.
20. Kim BK, Shin MS, Kim CJ, Baek SB, Ko YC, Kim YP. Treadmill exercise improves short-term memory by enhancing neurogenesis in amyloid beta-induced Alzheimer disease rats. J Exerc Rehabil. 2014;10(1):2-8.
21. Liu HL, Zhao G, Zhang H, Shi LD. Long-term treadmill exercise inhibits the progression of Alzheimer's disease-like neuropathology in the hippocampus of APP/PS1 transgenic mice. Behav Brain Res. 2013;256:261-272.
22. Kang EB, Kwon IS, Koo JH, et al. Treadmill exercise represses neuronal cell death and inflammation during Aβ-induced ER stress by regulating unfolded protein response in aged presenilin 2 mutant mice. Apoptosis. 2013;18(11):1332-1347.
23. Yaghoubi A, Saghebjoo M, Fallah Mohammadi Z, Hedayati M, Hajizadeh Moghaddam A. Effects of continuous training intensity on amyloid beta1-42(Aβ1-42) levels in hippocampus of homocysteine-induced alzheimer's model rats. J Arak Uni Med Sci 2016; 18 (11) :83-93.
24. Selkoe DJ, Hardy J. The amyloid hypothesis of Alzheimer's disease at 25 years. EMBO Mol Med. 2016; 1;8(6):595-608.
25. Gispen WH, Biessels GJ. Cognition and synaptic plasticity in diabetes mellitus. Trends Neurosci. 2000; 23(11):542-549.
26. Sojkova J, Zhou Y, An Y, Kraut MA, Ferrucci L, Wong DF, Resnick SM. Longitudinal patterns of β-amyloid deposition in nondemented older adults. Arch Neurol. 2011 May;68(5):644-9.
27. Butterfield DA, Sultana R. Methionine-35 of aβ(1-42): importance for oxidative stress in Alzheimer disease. J Amino Acids. 2011; 198430.
28. Glabe CC. Amyloid accumulation and pathogensis of Alzheimer's disease: significance of monomeric, oligomeric and fibrillar Abeta. Subcell Biochem. 2005;38:167-177.
29. Caspersen C, Wang N, Yao J, et al. Mitochondrial Abeta: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease. FASEB J. 2005;19(14):2040-2041.
30. Boyd-Kimball D, Sultana R, Mohmmad-Abdul H, Butterfield DA. Rodent Abeta(1-42) exhibits oxidative stress properties similar to those of human Abeta(1-42): Implications for proposed mechanisms of toxicity. J Alzheimers Dis. 2004;6(5):515-525.
31. Nishida N, Nagata N, Toda H, et al. Association of lipocalin-type prostaglandin D synthase with disproportionately enlarged subarachnoid-space in idiopathic normal pressure hydrocephalus. Fluids Barriers CNS. 2014;11(1):9.
32. Gomez-Casado E, Estepa A, Coll JM. A comparative review on European-farmed finfish RNA viruses and their vaccines [published correction appears in Vaccine. Vaccine. 2011; 29(15):2657-2671.
33. Viola KL, Klein WL. Amyloid β oligomers in Alzheimer's disease pathogenesis, treatment, and diagnosis. Acta Neuropathol. 2015;129(2):183-206.
34. Uslu S, Akarkarasu ZE, Ozbabalik D, et al. Levels of amyloid beta-42, interleukin-6 and tumor necrosis factor-alpha in Alzheimer's disease and vascular dementia. Neurochem Res. 2012;37(7):1554-1559.
35. Cavallucci V, D’Amelio M, Cecconi F. Aβ toxicity in Alzheimer's disease. Molecular neurobiology. 2012; 45:366-378.
36. Souza AD, Goto GO, Mainardi JA, Coelho AV, Tadini CC. Cassava starch composite films incorporated with cinnamon essential oil: Antimicrobial activity, microstructure, mechanical and barrier properties. LWT-Food Science and Technology. 2013; 54(2):346-352.
37. Paillard T, Rolland Y, de Souto Barreto P. Protective effects of physical exercise in alzheimer's disease and parkinson's disease: A Narrative Review. J Clin Neurol. 2015;11(3):212-9.
38. Liu Y, Liu F, Grundke-Iqbal I, Iqbal K, Gong CX. Deficient brain insulin signalling pathway in Alzheimer's disease and diabetes. J Pathol. 2011;225(1):54-62.
39. Liu F, Shi J, Tanimukai H, et al. Reduced O-GlcNAcylation links lower brain glucose metabolism and tau pathology in Alzheimer's disease. Brain. 2009;132(Pt 7):1820-1832.
40. Liu SJ, Wang JZ. Alzheimer-like tau phosphorylation induced by wortmannin in vivo and its attenuation by melatonin. Acta Pharmacol Sin. 2002;23(2):183-187.
41. Bhat RV, Budd Haeberlein SL, Avila J. Glycogen synthase kinase 3: a drug target for CNS therapies. J Neurochem. 2014; 89(6): 1313-7.
42. Paudel HK, Lew J, Ali Z, Wang JH. Brain proline-directed protein kinase phosphorylates tau on sites that are abnormally phosphorylated in tau associated with Alzheimer's paired helical filaments. J Biol Chem. 1993;268(31):23512-23518.
43. Hernandez F, Lucas JJ, Avila J. GSK3 and tau: two convergence points in Alzheimer's disease. J Alzheimers Dis. 2013; 33 1:S141-S144.
44. Pei JJ, Braak E, Braak H, et al. Distribution of active glycogen synthase kinase 3beta (GSK-3beta) in brains staged for Alzheimer disease neurofibrillary changes. J Neuropathol Exp Neurol. 1999;58(9):1010-1019.
45. Zhang Y, Zhang Z, Wang H, et al. Neuroprotective effect of ginsenoside Rg1 prevents cognitive impairment induced by isoflurane anesthesia in aged rats via antioxidant, anti-inflammatory and anti-apoptotic effects mediated by the PI3K/AKT/GSK-3β pathway. Mol Med Rep. 2016;14(3):2778-2784.
46. Biessels GJ, Reagan LP. Hippocampal insulin resistance and cognitivedysfunction. Nature reviews Neuroscience. 2015; 16:660.