Alzheimer’s disease (AD) is a multifactorial and chronic neurodegenerative disorder that interferes with memory, thinking, and behavior. The consumption of dietary fat has been considered a vital factor for AD as this disease is related to blood-brain barrier function and cholesterol signaling. The ε4 allele of apolipoprotein E (APOE4) is a primary genetic risk factor that encodes one of many proteins accountable for the transport of cholesterol and it is deemed as the leading cholesterol transport proteins in the brain. In case of AD development, the causative factor is the high level of serum/plasma cholesterol. However, this statement is arguable and, in the meantime, the levels of brain cholesterol in individuals with AD are extremely inconstant and levels of cholesterol in the brain and serum/plasma of AD individuals do not reflect cholesterol as a risk factor. In fact, APOE4 is neither fundamental nor sufficient for the advancement of AD; it just acts as a synergistic and increases the danger of AD. Another noticeable characteristic of AD is area-specific decreases in the metabolism of brain glucose. It has been found that the brain cells cannot efficiently metabolize fats; hence, they totally rely upon glucose as a vitality substrate. Thus, suppression of glucose metabolism can possess an intense effect on brain actions. Hypometabolism is frequently found in AD and has quite recently achieved impressive consideration as a plausible target for interfering in the progression of the disease. One promising approach is to keep up the normal supply of glucose to the brain with ketone bodies from the ketogenic diet signifies a potential therapeutic agent for AD. Therefore, this review represents the role of ketogenic diets to combat AD pathogenesis by considering the influence of APOE.

阿尔茨海默氏病（AD）是一种多因素和慢性神经退行性疾病，会干扰记忆，思维和行为。食用脂肪的摄入已被认为是AD的重要因素，因为该疾病与血脑屏障功能和胆固醇信号传导有关。载脂蛋白E（APOE4）的ε4等位基因）是主要的遗传危险因素，其编码负责胆固醇运输的许多蛋白质之一，被认为是大脑中主要的胆固醇运输蛋白质。如果发生AD，病因是血清/血浆胆固醇水平高。然而，这种说法是有争议的，与此同时，患有AD的个体的脑胆固醇水平非常不稳定，并且患有AD的个体的脑和血清/血浆中的胆固醇水平没有反映胆固醇是危险因素。实际上，APOE4对于AD的发展既不根本也不充分；它只是起到协同作用，增加了AD的危险。AD的另一个显着特征是脑葡萄糖代谢的区域特异性降低。已经发现脑细胞不能有效地代谢脂肪。因此，它们完全依赖葡萄糖作为活力的底物。因此，抑制葡萄糖代谢可以对脑部动作产生强烈影响。代谢低下症常见于AD，并且作为干扰疾病进展的合理靶点，近来已取得令人印象深刻的考虑。一种有前途的方法是保持生酮饮食中酮体向大脑的葡萄糖正常供应，这预示着AD的潜在治疗剂。因此，APOE。