Relationship between Amyloid-beta 42 Levels and Y-maze Alternation Values in Sprague Dawley Alzheimer’s Induction Received Medium-Chain Triglycerides Therapy
DOI:
https://doi.org/10.3889/oamjms.2020.3243Keywords:
Aβ-42, Y-maze, Medium-chain triglyceridesAbstract
BACKGROUND: At present, there is no pharmacological therapy that can cure Alzheimer’s disease. Treatment is only limited to preventing progression and controlling risk factors that worsen Alzheimer’s. Medium-chain triglycerides (MCT) are nutritional therapies that are being studied to prevent the progression of Alzheimer’s disease.
AIM: This study aims to see the effect of giving MCT to the value of percentage alternation Y-maze test and serum Aβ-42 levels as a marker of Alzheimer’s disease.
MATERIALS AND METHODS: This study is an experimental study using postp-test control group design. Samples from this study were 30 Sprague Dawley rats which were divided into positive control groups, negative controls, and three treatment groups. Positive control group and treatment were induced by Alzheimer’s by ovariectomy and d-galactose. After induction, MCT were given to the treatment group for 6 weeks. After treatment, the levels of Aβ-42 serum were examined by ELISA and cognitive function was examined by Y-maze. After that, the data were analyzed by ANOVA. p < 0.05 was said to be statistically significant.
RESULTS: The results showed that this study was found a moderate relationship with a positive pattern. This means that the higher the percentage alternation value, the higher the level of Aβ-42 in serum which indicates that the higher the percentage alternation value, the higher the clearance of Aβ-42.
CONCLUSION: This study concluded that the group of rats given MCT has a serum Aβ-42 level higher than the group of rats that were not given MCT.
Downloads
Metrics
Plum Analytics Artifact Widget Block
References
Dayrit FM. Lauric acid is a medium-chain fatty acid, coconut oil is a medium-chain triglyceride. Philipp J Sci. 2010;143(2):157-66.
Dean W, English J. Medium chain triglyserides: Beneficial effects on energi, atherosclerosis and aging. Nutr Rev. 2013.
Reger MA, Henderson ST, Hale C, Cholerton B, Baker LD, Watson GS, et al. Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. Neurobiol Aging. 2004;25(3):311-4. https://doi.org/10.1016/s0197-4580(03)00087-3 PMid:15123336 DOI: https://doi.org/10.1016/S0197-4580(03)00087-3
Ota M, Matsuo J, Ishida I, Hattori K, Teraishi T, Tonouchi H, et al. Effect of a ketogenic meal on cognitive function in elderly adults: Potential for cognitive enhancement. Psychopharmacology (Berl). 2016;233(21-22):3797-802. https://doi.org/10.1007/s00213-016-4414-7 PMid:27568199 DOI: https://doi.org/10.1007/s00213-016-4414-7
Zhang W, Hao J, Liu R, Zhang Z, Lei G, Su C, et al. Soluble Aβ levels correlate with cognitive deficits in the 12-month-old APPswe/PS1dE9 mouse model of Alzheimer’s disease. Behav Brain Res. 2011;222(2):342-50. https://doi.org/10.1016/j.bbr.2011.03.072 PMid:21513747 DOI: https://doi.org/10.1016/j.bbr.2011.03.072
Vassar R. BACE1 inhibitors drugs in clinical trials for Alzheimer’s disease. Biomed Central. Alzheimer’s research and therapy. Front Neuroendocrinol. 2014;29:507-9. https://doi.org/10.1186/s13195-014-0089-7 DOI: https://doi.org/10.1186/s13195-014-0089-7
Dong S, Duan Y, Hu Y, Zhao Z. Advances in the pathogenesis of Alzheimer’s disease: A re-evaluation of amyloid cascade hypothesis. Transl Neurodegener. 2012;1(1):18. https://doi.org/10.1186/2047-9158-1-18 PMid:23210692 DOI: https://doi.org/10.1186/2047-9158-1-18
Steiner H. Uncovering gamma-secretase. Curr Alzheimer Res. 2004;1(3):175-81. PMid:15975065 DOI: https://doi.org/10.2174/1567205043332081
Mawuenyega KG, Sigurdson W, Ovod V, Munsell L, Kasten T, Morris JC, et al. Decreased clearance of CNS beta-amyloid in Alzheimer’s disease. Science. 2010;330(6012):1774. https://doi.org/10.1126/science.1197623 PMid:21148344 DOI: https://doi.org/10.1126/science.1197623
Bertram L, Lill CM, Tanzi RE. The genetics of Alzheimer disease: Back to the future. Neuron. 2010;68(2):270-81. https://doi.org/10.1016/j.neuron.2010.10.013 PMid:20955934 DOI: https://doi.org/10.1016/j.neuron.2010.10.013
Marten B, Maria P, Jurgen S. Medium-chain triglyserides. Int Dairy J. 2006;16(11):1374-82. DOI: https://doi.org/10.1016/j.idairyj.2006.06.015
Ngatijdan. Petunjuk Laboratorium, Metode Laboratorium dalam Toksikologi. Yogyakarta: Pusat Antar Universitas Bioteknologi Universitas Gajah Mada; 2006. https://doi.org/10.20886/jpth.2010.4.3.157-165 DOI: https://doi.org/10.20886/jpth.2010.4.3.157-165
Momeni S, Segerström L, Roman E. Supplier-dependent differences in intermittent voluntary alcohol intake and response to naltrexone in Wistar rats. Front Neurosci. 2015;9:424. https://doi.org/10.3389/fnins.2015.00424 PMid:26594143 DOI: https://doi.org/10.3389/fnins.2015.00424
Studzinski CM, MacKay WA, Beckett TL, Henderson ST, Murphy MP, Sullivan PG, et al. Induction of ketosis may improve mitochondrial function and decrease steady-state amyloid-beta precursor protein (APP) levels in the aged dog. Brain Res. 2008;1226:209-17. https://doi.org/10.1016/j.brainres.2008.06.005 PMid:18582445 DOI: https://doi.org/10.1016/j.brainres.2008.06.005
Van der Auwera I, Wera S, Van Leuven F, Henderson ST. A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer’s disease. Nutr Metab (Lond). 2005;2:28. https://doi.org/10.1016/j.jalz.2006.05.2149 PMid:16229744 DOI: https://doi.org/10.1186/1743-7075-2-28
Croteau E, Castellano CA, Richard MA, Fortier M, Nugent S, Lepage M, et al. Ketogenic medium chain triglycerides increase brain energy metabolism in Alzheimer’s disease. J Alzheimers Dis. 2018;64(2):551-61. https://doi.org/10.3233/jad-180202 PMid:29914035 DOI: https://doi.org/10.3233/JAD-180202
Downloads
Published
How to Cite
License
Copyright (c) 2020 Faradila Faradila, Yuliarni Syafrita, Nur Indrawaty Lipoeto (Author)
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
http://creativecommons.org/licenses/by-nc/4.0