Oliveira, T.P.D.; Morais, A.L.B.; dos Reis, P.L.B.; Palotás, A.; Vieira, L.B. A Potential Role for the Ketogenic Diet in Alzheimer’s Disease Treatment: Exploring Pre-Clinical and Clinical Evidence. Metabolites2024, 14, 25.
Oliveira, T.P.D.; Morais, A.L.B.; dos Reis, P.L.B.; Palotás, A.; Vieira, L.B. A Potential Role for the Ketogenic Diet in Alzheimer’s Disease Treatment: Exploring Pre-Clinical and Clinical Evidence. Metabolites 2024, 14, 25.
Oliveira, T.P.D.; Morais, A.L.B.; dos Reis, P.L.B.; Palotás, A.; Vieira, L.B. A Potential Role for the Ketogenic Diet in Alzheimer’s Disease Treatment: Exploring Pre-Clinical and Clinical Evidence. Metabolites2024, 14, 25.
Oliveira, T.P.D.; Morais, A.L.B.; dos Reis, P.L.B.; Palotás, A.; Vieira, L.B. A Potential Role for the Ketogenic Diet in Alzheimer’s Disease Treatment: Exploring Pre-Clinical and Clinical Evidence. Metabolites 2024, 14, 25.
Abstract
Given the remarkable progress in global health and overall quality of life, the significant rise in life expectancy has become intertwined with the surging occurrence of neurodegenerative disorders (ND). This emerging trend is poised to pose a substantial challenge to the fields of medicine and public health in the years ahead. In this context, Alzheimer's disease (AD) is regarded as a ND that causes recent memory loss, motor impairment and cognitive deficits. AD is the most common cause of dementia in the elderly and its development is linked to multifactorial interac-tions between the environment, genetics, aging and lifestyle. The pathological hallmarks in AD are the accumulation of beta amyloid (A) peptide, the hyperphosphorylation of tau protein, neuro-toxic events and impaired glucose metabolism. Due to pharmacological limitations and in view of the prevailing glycemic hypometabolism, the ketogenic diet (KD) emerges as a promising non-pharmacological possibility for managing AD, an approach that has already demonstrated efficacy in addressing other disorders, notably epilepsy. KD consists of a food regimen in which carbohydrate intake is discouraged at the expense of increased lipid consumption, inducing met-abolic ketosis, whereby the main source of energy becomes ketone bodies, instead of glucose. Thus, under these dietary conditions, neuronal death through lack of energy would be decreased, inasmuch as the metabolism of lipids is not impaired in AD. In this way, the clinical picture of patients with AD would potentially improve, through the slowing down of symptoms and delaying the progression of the disease. Hence, this review aims to explore the rationale behind utilizing the KD in AD treatment while emphasizing the metabolic interplay between KD and the improvement of AD indicators, drawing insights from both pre-clinical and clinical investigations.
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
