Özet:

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 involved in the development of cognitive functions due to anti-inflammatory 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.

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