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Ketogenic Diet in Alzheimer's Disease


Ketogenic Diet in Alzheimer's Disease

Marta Rusek et al. Int J Mol Sci.


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.

Keywords: Alzheimer’s disease; amyloid; dementia; ketogenic diet; ketone bodies therapy; neuroinflammation; tau protein.

Conflict of interest statement

The authors declare no conflict of interest.


Figure 1
Figure 1
Hypothesized mechanisms through which ketogenic diet (KD) influence Alzheimer’s disease (AD) development. ↓—decreased; ↑—increased. Based on Reference [7].
Figure 2
Figure 2
Hypothetical pathways leading to the neuroprotective action of KD (based on References [50,108]). FA—fatty acids; GABA—γ-aminobutyric acid; PCr:Cr—phosphocreatine:creatine ratio; ROS—reactive oxygen species; UCP—uncoupling proteins; increase (↑) or decrease (↓)—arrows indicate the direction of the relationship between variables.

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    1. Patterson C. The World Alzheimer Report 2018: The State of the Art of Dementia Research: New Frontiers. Alzheimer’s Disease International (ADI); London, UK: Sep, 2018. [(accessed on 5 August 2019)]. Available online:
    1. Kelley B.J., Petersen R.C. Alzheimer’s disease and mild cognitive impairment. Neurol. Clin. 2007;25:577–609. doi: 10.1016/j.ncl.2007.03.008. - DOI - PMC - PubMed
    1. Lange K.W., Lange K.M., Makulska-Gertruda E., Nakamura Y., Reissmann A., Kanaya S., Hauser J. Ketogenic diets and Alzheimer’s disease. Food Sci. Hum. Wellness. 2017;6:1–9. doi: 10.1016/j.fshw.2016.10.003. - DOI
    1. Serrano-Pozo A., Frosch M.P., Masliah E., Hyman B.T. Neuropathological alterations in Alzheimer disease. Cold Spring Harb. Perspect. Med. 2011;1:a006189. doi: 10.1101/cshperspect.a006189. - DOI - PMC - PubMed
    1. Swerdlow R.H. Brain aging, Alzheimer’s disease, and mitochondria. Biochim. Biophys. Acta. 2011;1812:1630–1639. doi: 10.1016/j.bbadis.2011.08.012. - DOI - PMC - PubMed