Diyet Yağlarının Alzheimer Hastalığı Patolojisi Üzerine Potansiyel Koruyucu Etkileri

Yıl 2018, Cilt: 9 Sayı: 2, 141 - 149, 01.08.2018

Mustafa Fevzi Karagöz , Nilüfer Acar Tek

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.

Anahtar Kelimeler

Alzheimer hastalığı, omega 3 yağ asitleri, yağ asitleri kısa zincirli

Potential Protective Effects of Dietary Fats on The Pathogenesis of Alzheimer Disease

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.

Anahtar Kelimeler

Alzheimer’s disease, , omega 3 fatty acids, fatty acids short-chain

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.
• 42. Cecchi C, Nichino D, Zampagni M, Bernacchioni C, Evangelisti E, Pensalfini A, et al. A protective role for lipid raft cholesterol against amyloid-induced membrane damage in human neuroblastoma cells. Biochim Biophys Acta - Biomembr 2009; 1788(10): 2204–16.
• 43. Ledesma MD, Dotti CG. The conflicting role of brain cholesterol in Alzheimer’s disease: lessons from the brain plasminogen system. Biochem Soc Symp 2005; 72: 129–38.
• 44. Crichton GE, Elias MF, Davey A, Sullivan KJ, Robbins MA. Higher HDL Cholesterol Is Associated with Better Cognitive Function: the Maine-Syracuse Study. J Int Neuropsychol Soc 2014; 20(10): 961–70.
• 45. Wang D, Zheng W. Dietary cholesterol concentration affects synaptic plasticity and dendrite spine morphology of rabbit hippocampal neurons. Brain Res 2015; 1622: 350–60.
• 46. Solomon A, Kivipelto M, Wolozin B, Zhou J, Whitmer RA. Midlife serum cholesterol and increased risk of Alzheimer’s and vascular dementia three decades later. Dement Geriatr Cogn Disord 2009; 28(1): 75–80.
• 47. Alonso A, Jacobs DR, Menotti A, Nissinen A, Dontas A, Kafatos A, et al. Cardiovascular risk factors and dementia mortality: 40 years of follow-up in the Seven Countries Study. J Neurol Sci 2009; 280(1–2): 79–83.
• 48. Hughes T, Ganguli M. Modifiable Midlife Risk Factors for Late-Life Cognitive Impairment and Dementia. Curr Psychiatry Rev [Internet]. 2009 [cited 2018 Mar 23]; 5(2): 73–92. Available from: http://www.eurekaselect.com/openurl/content.php?genre=article&issn=1573-4005&volume=5&issue=2&spage=73
• 49. Lim WLF, Lam SM, Shui G, Mondal A, Ong D, Duan X, et al. Effects of a high-fat, high-cholesterol diet on brain lipid profiles in apolipoprotein E ɛ3 and ɛ4 knock-in mice. Neurobiol Aging 2013; 34(9): 2217–24.
• 50. Pensalfini A, Zampagni M, Liguri G, Becatti M, Evangelisti E, Fiorillo C, et al. Membrane cholesterol enrichment prevents Aβ-induced oxidative stress in Alzheimer’s fibroblasts. Neurobiol Aging 2011; 32: 210–22.
• 51. Leduc V, Jasmin-Bélanger S, Poirier J. APOE and cholesterol homeostasis in Alzheimer’s disease. Trends Mol Med 2010; 16(10): 469–77.
• 52. Grant WB. Trends in Diet and Alzheimer’s Disease During the Nutrition Transition in Japan and Developing Countries. J Alzheimer’s Dis 2014; 38(3): 611–20.
• 53. Singh B, Parsaik AK, Mielke MM, Erwin PJ, Knopman DS, Petersen RC, et al. Association of Mediterranean Diet with Mild Cognitive Impairment and Alzheimer’s Disease: A Systematic Review and Meta-Analysis. J Alzheimer’s Dis 2014; 39(2): 271–82.
• 54. Lane-Donovan C, Herz J. High-Fat Diet Changes Hippocampal Apolipoprotein E (ApoE) in a Genotype- and Carbohydrate-Dependent Manner in Mice. PLoS One [Internet]. 2016; 11(2): e0148099. Available from: http://dx.doi.org/10.1371%2Fjournal.pone.0148099
• 55. Baierle M, Vencato P, Oldenburg L, Bordignon S, Zibetti M, Trentini C, et al. Fatty Acid Status and Its Relationship to Cognitive Decline and Homocysteine Levels in the Elderly. Nutrients 2014; 6(9): 3624–40.
• 56. Schmitz G, Ecker J. The opposing effects of n−3 and n−6 fatty acids. Prog Lipid Res [Internet] 2008 Mar [cited 2018 Apr 3]; 47(2): 147–55. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18198131
• 57. Briante R, Febbraio F, Roberto N. Antioxidant Properties of Low Molecular Weight Phenols Present in the Mediterranean Diet. J Agric Food Chem 2003; 51(24): 6975–81.
• 58. Naqvi AZ, Harty B, Mukamal KJ, Stoddard AM, Vitolins M, Dunn JE. Monounsaturated, Trans, and Saturated Fatty Acids and Cognitive Decline in Women. J Am Geriatr Soc 2011; 59(5): 837–43.
• 59. Paoli A, Bianco A, Damiani E, Bosco G. Ketogenic diet in neuromuscular and neurodegenerative diseases. Biomed Res Int 2014; 2014: 474296.
• 60. Kashiwaya Y, Bergman C, Lee J-H, Wan R, King MT, Mughal MR, et al. A ketone ester diet exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and tau pathologies in a mouse model of Alzheimer’s disease. Neurobiol Aging 2013; 34(6): 1530–9.
• 61. 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-β precursor protein (APP) levels in the aged dog. Brain Res 2008; 1226: 209–17.
• 62. Hashim SA, VanItallie TB. Ketone body therapy: from the ketogenic diet to the oral administration of ketone ester. J Lipid Res 2014; 55(9): 1818–26.