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Diyet Yağlarının Alzheimer Hastalığı Patolojisi Üzerine Potansiyel Koruyucu Etkileri

Year 2018, Volume: 9 Issue: 2, 141 - 149, 01.08.2018
https://doi.org/10.22312/sdusbed.412464

Abstract

Alzheimer
hastalığı ilerleyici hafıza kaybı tablosuyla karakterize nörodejeneratif bir
hastalıktır. Öz bakım becerilerinde, bilişsel işlevlerinde yetersizlikler
görülmektedir. Patolojik olarak amiloid plaklarla özdeşleşmiş olsalar da tau
proteininin aşırı fosforillenmesi ve buna bağlı nörofibriler yumak oluşumu,
nöron kaybı Alzheimer hastalığı ile birlikte görülebilmektedir. Amiloid
plakların, tau proteinlerinin olumsuz etkisi, oksidatif strese yol açması,
glukoz homeostazının bozulması gibi birçok nedenden kaynaklanabilmektedir.
Patolojilere karşı geliştirilen tedavi yöntemleri de çeşitli olabilmektedir.
Oksidatif strese karşı antioksidanlardan zengin
beslenme, glukoz metabolizmasının bozulmasına karşı ketojenik diyet uygulamaları
Alzheimer hastalığının diyet tedavisi içinde yer almaktadır. Orta zincirli yağ
asitlerinin portal dolaşımdan hızlıca emilmeleri, β-oksidasyona ihtiyaç duymaksızın
alternatif enerji kaynağı olarak kullanılabilmesini sağlamaktadır. Ayrıca uzun zincirli n-3 grubu yağ asitlerinden eikosapentaenoik
asit (EPA) ve dekozahekzoenoik asit (DHA) antiinflamatuvar etkilerinden dolayı
bilişsel işlevleri geliştirici etkide bulunmaktadır. Bu derlemede Alzheimer
hastalığından korunmada, ilerlemesinin geciktirilmesinde ve hastalığın
tedavisinde yağ asitlerinin metabolik süreçlerdeki etkileri irdelenmiştir.

References

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  • 7. Tramutola A, Lanzillotta C, Perluigi M, Butterfield DA. Oxidative stress, protein modification and Alzheimer disease. Brain Res Bull 2017; 133: 88-96.
  • 8. Wojtunik-Kulesza KA, Oniszczuk A, Oniszczuk T, Waksmundzka-Hajnos M. The influence of common free radicals and antioxidants on development of Alzheimer’s Disease. Biomed Pharmacother 2016; 78: 39–49.
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Potential Protective Effects of Dietary Fats on The Pathogenesis of Alzheimer Disease

Year 2018, Volume: 9 Issue: 2, 141 - 149, 01.08.2018
https://doi.org/10.22312/sdusbed.412464

Abstract

Alzheimer's
disease is a neurodegenerative disorder characterized by a progressive memory
loss table. Self-care skills and cognitive functions are seen insufficiency.

Although
pathologically identified with amyloid plaques, excessive phosphorylation of
the tau protein and consequent neurofibrillary tangle formation, and neuronal
loss may be associated with Alzheimer's disease. Negative effects of amyloid
plaques and tau proteins can result in many causes such as oxidative stress,
impaired glucose homeostasis. Treatment methods developed against pathogens can
also be varied. A diet rich in antioxidants against oxidative stress, ketogenic
diet versus the deterioration of glucose metabolism in Alzheimer's is located
in the dietary treatment of disease. Rapid absorption of medium chain fatty
acids from the portal circulation ensures that they can be used as an
alternative energy source without the need for β-oxidation. In addition,
eicosapentaenoic acid (EPA) and decozahexenoic acid (DHA) of long chain n-3
fatty acids have been implicated in the development of cognitive functions due
to antiinflammatory effects. In this review, it has been examined that the
effects of fatty acids on metabolic processes in Alzheimer's disease, delayed
progression and treatment of disease.

References

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  • 3. Williams JW, Plassman BL, Burke J, Holsinger T, Benjamin S. Preventing Alzheimer’s disease and cognitive decline. Evid Rep Technol Assess (Full Rep) 2010; 193: 1–727.
  • 4. Toda N, Okamura T. Cigarette smoking impairs nitric oxide-mediated cerebral blood flow increase: Implications for Alzheimer’s disease. J Pharmacol Sci 2016; 131(4): 223–32.
  • 5. Herbert J, Lucassen PJ. Depression as a risk factor for Alzheimer’s disease: Genes, steroids, cytokines and neurogenesis - What do we need to know? Front Neuroendocr 2016; 41: 153–71.
  • 6. Hickman RA, Faustin A, Wisniewski T. Alzheimer Disease and Its Growing Epidemic: Risk Factors, Biomarkers, and the Urgent Need for Therapeutics. Neurol Clin 2016; 34(4): 941–53.
  • 7. Tramutola A, Lanzillotta C, Perluigi M, Butterfield DA. Oxidative stress, protein modification and Alzheimer disease. Brain Res Bull 2017; 133: 88-96.
  • 8. Wojtunik-Kulesza KA, Oniszczuk A, Oniszczuk T, Waksmundzka-Hajnos M. The influence of common free radicals and antioxidants on development of Alzheimer’s Disease. Biomed Pharmacother 2016; 78: 39–49.
  • 9. Luchsinger JA, Tang MX, Miller J, Green R, Mayeux R. Relation of higher folate intake to lower risk of Alzheimer disease in the elderly. Arch Neurol 2007; 64(1): 86–92.
  • 10. Ravaglia G, Forti P, Maioli F, Martelli M, Servadei L, Brunetti N, et al. Homocysteine and folate as risk factors for dementia and Alzheimer disease. Am J Clin Nutr 2005; 82(3): 636–43.
  • 11. Agrawal R, Gomez-Pinilla F. “Metabolic syndrome” in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition. J Physiol 2012; 590(Pt 10): 2485–99.
  • 12. Fotuhi M, Mohassel P, Yaffe K. Fish consumption, long-chain omega-3 fatty acids and risk of cognitive decline or Alzheimer disease: a complex association. Nat Clin Pr Neurol 2009; 5(3): 140–52.
  • 13. Kumar A, Singh A, Ekavali. A review on Alzheimer’s disease pathophysiology and its management: an update. Pharmacol Rep 2015; 67(2): 195–203.
  • 14. Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 1991; 82(4): 239–59.
  • 15. Esen S. Alzheimer Hastalığı Patofizyolojisi: Deneysel ve Genetik Bulgular. Turkish Journal Of Geriatrics 2010; 13(3): 21-26
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  • 17. Bird TD, Miller BL. Alzheimer’s disease and other dementias. In: Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw-Hill Medical Pub. Division, 2005; p. 2393–2406.
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  • 20. Gandy S. The role of cerebral amyloid beta accumulation in common forms of Alzheimer disease. J Clin Invest 2005; 115(5): 1121–9.
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  • 25. Benveniste EN, Nguyen VT, O’Keefe GM. Immunological aspects of microglia: relevance to Alzheimer’s disease. Neurochem Int [Internet] 2001 [cited 2017 Jan 19]; 39(5–6): 381–91. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11578773
  • 26. Davis KL. Alzheimer’s disease: seeking new ways to preserve brain function. Interview by Alice V. Luddington. Geriatrics [Internet] 1999 Feb [cited 2017 Jan 19]; 54(2): 42–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10024872
  • 27. Fernando WMADB, Rainey-Smith SR, Martins IJ, Martins RN. IN VITRO STUDY TO ASSESS THE POTENTIAL OF SHORT CHAIN FATTY ACIDS (SCFA) AS THERAPEUTIC AGENTS FOR ALZHEIMER’S DISEASE. Alzheimer’s Dement [Internet] 2014 [cited 2018 Mar 23]; 10(4):P626. Available from: http://linkinghub.elsevier.com/retrieve/pii/S1552526014017300
  • 28. Dinkova-Kostova AT, Kostov RV. Glucosinolates and isothiocyanates in health and disease. Trends Mol Med [Internet] 2012 [cited 2018 Mar 23]; 18(6): 337–47. Available from: https://www.sciencedirect.com/science/article/pii/S147149141200055X
  • 29. Yin F, Sancheti H, Patil I, Cadenas E. Energy metabolism and inflammation in brain aging and Alzheimer’s disease. Free Radic Biol Med [Internet] 2016 [cited 2018 Mar 23]; 100: 108–22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/27154981
  • 30. Ruiz HH, Chi T, Shin AC, Lindtner C, Hsieh W, Ehrlich M, et al. Increased susceptibility to metabolic dysregulation in a mouse model of Alzheimer’s disease is associated with impaired hypothalamic insulin signaling and elevated BCAA levels. Alzheimer’s Dement [Internet] 2016 [cited 2018 Mar 23]; 12(8): 851–61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26928090
  • 31. Lei E, Vacy K, Boon WC. Fatty acids and their therapeutic potential in neurological disorders. Neurochem Int [Internet] 2016 May [cited 2018 Mar 23]; 95: 75–84. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26939763
  • 32. Bianca Velasco A, Tan ZS. Fatty Acids and the Aging Brain. In: Watson RR, De Meester F, editors. Omega-3 Fatty Acids in Brain and Neurological Health. Amsterdam, Boston, Heidelberg, London, New York, Oxford, Paris, San Diego, San Francisco, Singapore, Sydney, Tokyo, Elsevier; 2014 p. 201–19.
  • 33. Hooijmans CR, Kiliaan AJ. Fatty acids, lipid metabolism and Alzheimer pathology. Eur J Pharmacol [Internet] 2008 [cited 2018 Mar 23]; 585(1): 176–96. Available from: https://www.sciencedirect.com/science/article/pii/S001429990800229X
  • 34. Solfrizzi V, D’Introno A, Colacicco AM, Capurso C, Del Parigi A, Capurso S, et al. Dietary fatty acids intake: possible role in cognitive decline and dementia. Exp Gerontol [Internet] 2005 [cited 2018 Mar 23]; 40(4): 257–70. Available from: https://www.sciencedirect.com/science/article/pii/S0531556505000094
  • 35. Simopoulos AP. Evolutionary Aspects of Diet: The Omega-6/Omega-3 Ratio and the Brain. Mol Neurobiol 2011; 44(2): 203–15.
  • 36. Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother 2002; 56(8): 365–79.
  • 37. Fernando WMADB, Martins IJ, Goozee KG, Brennan CS, Jayasena V, Martins RN. The role of dietary coconut for the prevention and treatment of Alzheimer’s disease: potential mechanisms of action. Br J Nutr 2015; 114(1): 1–14.
  • 38. Hashimoto M, Hossain S, Shimada T, Shido O. DOCOSAHEXAENOIC ACID-INDUCED PROTECTIVE EFFECT AGAINST IMPAIRED LEARNING IN AMYLOID ?-INFUSED RATS IS ASSOCIATED WITH INCREASED SYNAPTOSOMAL MEMBRANE FLUIDITY. Clin Exp Pharmacol Physiol 2006; 33(10): 934–9.
  • 39. Yurko-Mauro K, Alexander DD, Van Elswyk ME. Docosahexaenoic Acid and Adult Memory: A Systematic Review and Meta-Analysis. PLoS One 2015; 10(3): e0120391.
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There are 61 citations in total.

Details

Primary Language Turkish
Subjects Health Care Administration
Journal Section Derlemeler
Authors

Mustafa Fevzi Karagöz 0000-0003-1808-2748

Nilüfer Acar Tek

Publication Date August 1, 2018
Submission Date April 4, 2018
Published in Issue Year 2018 Volume: 9 Issue: 2

Cite

Vancouver Karagöz MF, Acar Tek N. Diyet Yağlarının Alzheimer Hastalığı Patolojisi Üzerine Potansiyel Koruyucu Etkileri. Süleyman Demirel Üniversitesi Sağlık Bilimleri Dergisi. 2018;9(2):141-9.

SDÜ Sağlık Bilimleri Dergisi, makalenin gönderilmesi ve yayınlanması dahil olmak üzere hiçbir aşamada herhangi bir ücret talep etmemektedir. Dergimiz, bilimsel araştırmaları okuyucuya ücretsiz sunmanın bilginin küresel paylaşımını artıracağı ilkesini benimseyerek, içeriğine anında açık erişim sağlamaktadır.