What is it about?

This article is based on the theory that Alzheimer's disease is caused by a pathological neuronal inability to use glucose as a fuel; a situation analogous to type 2 diabetes in the body. This causes the neurons to starve and degrade; resulting in Alzheimer's disease. In theory, therefore, providing the starving neurons with an alternative fuel (ketones) may alleviate symptoms. This article reviews six human studies in which a state of ketosis was induced though a low-carbohydrate diet or administration of exogenous ketones, and cognitive performance measured. The results provide promising evidence that keto-neuro-therapy may be an important and effective therapeutic and preventative intervention in the fight against this disease.

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Why is it important?

Carriers of one or more copy of the ApoE4 allele responded significantly worse than those without, allowing for discussion of the link between genetics and AD. In the genotypic analyses of Henderson et al (2009) and Henderson and Poirier (2011), the intervention had little effect on carriers of E4. This suggests that E4 carriers are impaired in neuronal ability to metabolise ketones, an implication that may facilitate an understanding of the link between E4 and the aetiology of AD. The APOE gene regulates cholesterol absorption, lipid transport and serum lipoprotein metabolism (Corbo and Scacchi, 1999). Despite its notorious connection with AD, Corbo and Scacchi (1999) propose that this ancient allele conferred advantages in foraging communities where food was scarce by increasing intestinal cholesterol absorption and plasma levels. Therefore, its carriage was advantageous for our ‘Palaeolithic’ ancestors, who ate an unprocessed, naturally lower-carbohydrate diet. Henderson (2004) proposed that the ‘Neolithic’ diet, which followed the agricultural revolution, altered the human macronutrient profile by elevating carbohydrate consumption, creating a discordance between allele and diet, and that the high-carbohydrate diet is the primary cause of AD for all genotypes, but particularly damaging to those with E4. This is because both the ApoE4 allele and a high-carbohydrate diet induce similar effects (Henderson, 2004), increasing levels of low-density lipoprotein (LDL) and total cholesterol (Corbo and Scacchi, 1999) and suppressing lipid metabolism (Henderson, 2004).


Future research could explore the relationship between the common symptom of glucose craving in Alzheimer's disease and cerebral hypometabolism of glucose.

Karyn Brackley
Bournemouth University

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This page is a summary of: The cerebral hypometabolism model of Alzheimer's disease explored: can a ketogenic diet improve cognition in Alzheimer's disease? A review of the literature, British Journal of Neuroscience Nursing, June 2021, Mark Allen Group,
DOI: 10.12968/bjnn.2021.17.3.95.
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