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Diyet Yağlarının Alzheimer Hastalığı Patolojisi Üzerine Potansiyel Koruyucu Etkileri

Yıl 2018, Cilt 9, Sayı 2, 141 - 149, 01.08.2018
https://doi.org/10.22312/sdusbed.412464

Öz

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.

Kaynakça

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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
  • 16. Öztürk GB, Karan MA. Alzheimer Hastalığının Fizyopatolojisi. Klin Gelişim. 2009; 22: 32–46.
  • 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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  • 19. Bennett DA, Schneider JA, Wilson RS, Bienias JL, Arnold SE. Neurofibrillary tangles mediate the association of amyloid load with clinical Alzheimer disease and level of cognitive function. Arch Neurol 2004; 61(3): 378–84.
  • 20. Gandy S. The role of cerebral amyloid beta accumulation in common forms of Alzheimer disease. J Clin Invest 2005; 115(5): 1121–9.
  • 21. Georganopoulou DG, Chang L, Nam JM, Thaxton CS, Mufson EJ, Klein WL, et al. Nanoparticle-based detection in cerebral spinal fluid of a soluble pathogenic biomarker for Alzheimer’s disease. Proc Natl Acad Sci U S A 2005; 102(7): 2273–6.
  • 22. Rissman RA, Poon WW, Blurton-Jones M, Oddo S, Torp R, Vitek MP, et al. Caspase-cleavage of tau is an early event in Alzheimer disease tangle pathology. J Clin Invest [Internet] 2004 Jul 1 [cited 2017 Jan 19]; 114(1): 121–30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15232619
  • 23. Spillantini MG, Murrell JR, Goedert M, Farlow MR, Klug A, Ghetti B. Mutation in the tau gene in familial multiple system tauopathy with presenile dementia. Proc Natl Acad Sci U S A [Internet] 1998 [cited 2017 Jan 19]; 95(13): 7737–41. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9636220
  • 24. Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and Alzheimer’s disease. Neurobiol Aging [Internet] 2000 [cited 2017 Jan 19]; 21(3): 383–421. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10858586
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  • 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
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  • 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.
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Potential Protective Effects of Dietary Fats on The Pathogenesis of Alzheimer Disease

Yıl 2018, Cilt 9, Sayı 2, 141 - 149, 01.08.2018
https://doi.org/10.22312/sdusbed.412464

Öz

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.

Kaynakça

  • 1. Blennow K, de Leon MJ, Zetterberg H. Alzheimer’s disease. Lancet. 2006; 368(9533): 387–403. 2. Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM. Forecasting the global burden of Alzheimer’s disease. Alzheimers Dement 2007; 3(3): 186–91.
  • 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
  • 16. Öztürk GB, Karan MA. Alzheimer Hastalığının Fizyopatolojisi. Klin Gelişim. 2009; 22: 32–46.
  • 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.
  • 18. Näslund J, Haroutunian V, Mohs R, Davis KL, Davies P, Greengard P, et al. Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline. JAMA [Internet] 2000 [cited 2017 Jan 19]; 283(12): 1571–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10735393
  • 19. Bennett DA, Schneider JA, Wilson RS, Bienias JL, Arnold SE. Neurofibrillary tangles mediate the association of amyloid load with clinical Alzheimer disease and level of cognitive function. Arch Neurol 2004; 61(3): 378–84.
  • 20. Gandy S. The role of cerebral amyloid beta accumulation in common forms of Alzheimer disease. J Clin Invest 2005; 115(5): 1121–9.
  • 21. Georganopoulou DG, Chang L, Nam JM, Thaxton CS, Mufson EJ, Klein WL, et al. Nanoparticle-based detection in cerebral spinal fluid of a soluble pathogenic biomarker for Alzheimer’s disease. Proc Natl Acad Sci U S A 2005; 102(7): 2273–6.
  • 22. Rissman RA, Poon WW, Blurton-Jones M, Oddo S, Torp R, Vitek MP, et al. Caspase-cleavage of tau is an early event in Alzheimer disease tangle pathology. J Clin Invest [Internet] 2004 Jul 1 [cited 2017 Jan 19]; 114(1): 121–30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15232619
  • 23. Spillantini MG, Murrell JR, Goedert M, Farlow MR, Klug A, Ghetti B. Mutation in the tau gene in familial multiple system tauopathy with presenile dementia. Proc Natl Acad Sci U S A [Internet] 1998 [cited 2017 Jan 19]; 95(13): 7737–41. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9636220
  • 24. Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and Alzheimer’s disease. Neurobiol Aging [Internet] 2000 [cited 2017 Jan 19]; 21(3): 383–421. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10858586
  • 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.
  • 40. National Institutes of Health (NIH) [Internet]. [cited 2018 Mar 23]. Available from: https://ods.od.nih.gov/factsheets/Omega3FattyAcids-HealthProfessional/
  • 41. Sparks DL, Scheff SW, Hunsaker JC, Liu H, Landers T, Gross DR. Induction of Alzheimer-like β-Amyloid Immunoreactivity in the Brains of Rabbits with Dietary Cholesterol. Exp Neurol 1994; 126(1): 88–94.
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Ayrıntılar

Birincil Dil Türkçe
Konular Sağlık Bilimleri ve Hizmetleri
Bölüm Derlemeler
Yazarlar

Mustafa Fevzi KARAGÖZ> (Sorumlu Yazar)
Gazi University,Ankara,Turkey
0000-0003-1808-2748
Türkiye


Nilüfer ACAR TEK>
Gazi University,Ankara,Turkey
Türkiye

Yayımlanma Tarihi 1 Ağustos 2018
Başvuru Tarihi 4 Nisan 2018
Kabul Tarihi 16 Ağustos 2018
Yayınlandığı Sayı Yıl 2018, Cilt 9, Sayı 2

Kaynak Göster

Vancouver Karagöz M. F. , Acar Tek N. Diyet Yağlarının Alzheimer Hastalığı Patolojisi Üzerine Potansiyel Koruyucu Etkileri. Süleyman Demirel Üniversitesi Sağlık Bilimleri Dergisi. 2018; 9(2): 141-149.

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.