Abstract
The ketogenic diet, originally developed for the treatment of epilepsy in non-responder children, is spreading to be used in the treatment of many diseases, including Alzheimer’s disease. The main activity of the ketogenic diet has been related to improved mitochondrial function and decreased oxidative stress. B-Hydroxybutyrate, the most studied ketone body, has been shown to reduce the production of reactive oxygen species (ROS), improving mitochondrial respiration: it stimulates the cellular endogenous antioxidant system with the activation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2), it modulates the ratio between the oxidized and reduced forms of nicotinamide adenine dinucleotide (NAD+/NADH) and it increases the efficiency of electron transport chain through the expression of uncoupling proteins. Furthermore, the ketogenic diet performs anti-inflammatory activity by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) activation and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome as well as inhibiting histone deacetylases (HDACs), improving memory encoding. The underlying mechanisms and the perspectives for the treatment of Alzheimer’s disease are discussed.
Highlights
According to the World Alzheimer Report 2016, there are 47 million people worldwide suffering from dementia, and this number will rise to 131 million by 2050 due to population aging
When there is a decreased expression of these transporters, as it has been shown in Alzheimer’s disease (AD), Ketone Bodies (KBs) become the alternative energy source to glucose for the brain due to their ability to cross the blood-brain barrier (BBB) carried by specific transporters that are not down-regulated during AD
Both diets significantly decreased the concentration of several serum inflammatory markers, but there was an overall greater anti-inflammatory effect associated with ketogenic diet (KD): a larger reduction was observed in TNF-alpha, interleukin-8 (IL-8), monocyte chemoattractant protein (MCP-1), plasminogen activator inhibitor-1 (PAI-1), E-selectin, intercellular adhesion molecule-1 (ICAM-1), while these markers showed a little change in the subjects fed with a low fat diet, suggesting that it is the macronutrient composition, not the weight loss or the caloric reduction the real responsible for the anti-inflammatory activity [102]
Summary
According to the World Alzheimer Report 2016, there are 47 million people worldwide suffering from dementia, and this number will rise to 131 million by 2050 due to population aging. When there is a decreased expression of these transporters, as it has been shown in AD, Ketone Bodies (KBs) become the alternative energy source to glucose for the brain due to their ability to cross the BBB carried by specific transporters that are not down-regulated during AD. For all these reasons many studies have been performed to verify if the induction of a mild ketosis may favor the trophism of neuronal cells in the course of AD. The aim of this review is to summarize the current evidence regarding KD and AD with specific reference to antioxidant and anti-inflammatory mechanisms, as well as their effects on cognitive processes
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