Introduction: Alzheimer’s disease (AD) is the most common cause of dementia, affecting more than 10% of people over 65. It could be concluded that up to date, we know many mechanisms that could affect the setup and progress of AD pathogenesis. It seems like AD is not only one or two types of disease, but it could be a group of diseases with similar APP and Tau pathologies triggered by different mechanisms. Genetic disposition to AD would play an important role in the mechanisms of Alzheimer’s disease initiations. Also, Aging, head injuries, vascular diseases, infections, Changes in metabolism, and environmental factors play a role in this disease
Methods: The human brain requires a significant amount of energy to function normally and accounts for about 20% of the body's total energy expenditure at rest, even though the brain makes up only 2% of the total body weight in addition to energy. Other cellular processes, such as cytoskeleton remodeling, phospholipid synthesis, and axonal transport, require ATP for neural signaling. Therefore, an adequate and continuous energy supply is essential to maintain brain cellular function. Furthermore, today, research focuses on understanding AD pathology by targeting mechanisms such as energy changes resulting from metabolism, amyloid β, and inflammatory response. In this review, we want to check if Alzheimer's disease affects on metabolism. What are these effects?
Results: Overproduction or reduced clearance of Ab peptides in the brain plays a central role in the pathogenesis of AD. Understanding the changes in body metabolism that can affect brain AB levels is critical to developing treatments to reduce the incidence of AD. Almost every aspect of lipid metabolism, especially cholesterol, is related to Ab production, Ab clearance, or AD risk. Also, changes in the energy level related to glucose, ketogenesis, etc. are effective in Alzheimer's disease
Conclusion: Alzheimer's disease (AD) is initially characterized by the deposition revealed in patients with AD, characterized by the presence of nerve cells and loss of synaptic cells in this disease. The death of nerve cells is because of a peptide of 40-43 amino acids called peptide (AB) beta-amyloid, which causes the nerve cells to die. The toxicity is high. Now the question arises, what is the reason for their resistance? It was observed that these cells do not respond to high concentrations of AB in amyloid toxicity by inhibiting growth or by accumulating peroxides. These resistant cells express a much higher level of antioxidant enzymes catalase and glutathione peroxidase (GPX). A change in ROS metabolism is a significant component of AB toxicity. AB-resistant cells have been shown to have high levels of G6PDH and NADPH, increased glucose flux through the shunt pathway, and elevated glycolysis and pentose activities. These AB-resistant clones also strongly reduce ROS levels. For example, laboratory studies showed that Aβ activates the hydrolysis of sphingomyelin and causes the accumulation of ceramide. Ceramide, in turn, affects the production of Aβ by releasing beta and promoting the amyloidogenic pathway. Also, during Alzheimer's, there are changes in the energy level of cholesterol and other lipids, which causes a change in the level of ROS and increases the incidence of AD.