Abstract
At present, the prevalence of Alzheimer’s disease, a devastating neurodegenerative disorder, is increasing. Although the mechanism of the underlying pathology is not fully uncovered, in the last years, there has been significant progress in its understanding. This includes: Progressive deposition of amyloid β-peptides in amyloid plaques and hyperphosphorylated tau protein in intracellular as neurofibrillary tangles; neuronal loss; and impaired glucose metabolism. Due to a lack of effective prevention and treatment strategy, emerging evidence suggests that dietary and metabolic interventions could potentially target these issues. The ketogenic diet is a very high-fat, low-carbohydrate diet, which has a fasting-like effect bringing the body into a state of ketosis. The presence of ketone bodies has a neuroprotective impact on aging brain cells. Moreover, their production may enhance mitochondrial function, reduce the expression of inflammatory and apoptotic mediators. Thus, it has gained interest as a potential therapy for neurodegenerative disorders like Alzheimer’s disease. This review aims to examine the role of the ketogenic diet in Alzheimer’s disease progression and to outline specific aspects of the nutritional profile providing a rationale for the implementation of dietary interventions as a therapeutic strategy for Alzheimer’s disease.
Highlights
Alzheimer’s disease (AD) is the most significant cause of dementia that affects around 50 million people worldwide [1]
This review summarizes the experimental and clinical data, which suggest that the ketogenic diet could be a potential therapy option for AD, due to its neuroprotective properties
Abnormal glucose metabolism uptake, diminished mitochondrial-associated brain energy metabolism, changes in neurotransmitter release, and increased inflammatory response are the key pathophysiological metabolic alterations observed in AD
Summary
Alzheimer’s disease (AD) is the most significant cause of dementia that affects around 50 million people worldwide [1]. It is a heterogeneous and multifactorial disorder, characterized by cognitive impairment with a progressive decline in memory, disorientation, impaired self-care, and personality changes [2,3]. Cognitive deficits, resulting from the loss of neurons, are susceptible to neurofibrillary degeneration located in the limbic system, subcortical structures, archicortex and neocortex, and progressive synaptic dysfunction [4]. AD involves progressive deposition of amyloid β-peptide (Aβ) as amyloid plaques, hyperphosphorylated tau protein intracellularly as neurofibrillary tangles (NFTs) and neuronal loss in the hippocampus [2]. Patients with AD present mitochondrial dysfunction and metabolic changes, such as impaired glucose utilization in the brain (glucose hypometabolism) [5]
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