{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T16:17:31Z","timestamp":1777393051140,"version":"3.51.4"},"reference-count":62,"publisher":"SAGE Publications","issue":"s1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2024,10,18]]},"abstract":"<jats:p>Dementia represents one of the largest and most urgent public health problems across the globe. Modeling projections have estimated that delaying the onset of Alzheimer\u2019s disease (AD) by 6 months would reduce the prevalence by 5%, while a delay of 12 months would reduce the prevalence by 10%. One approach to achieving a delay in the onset of AD is to investigate lifestyle interventions that could be widely implemented with a favorable risk-benefit relationship and socioeconomic profile. Amongst such interventions, there is increasing evidence to support the use of ketogenic interventions in AD. Indeed, it is well known that cerebral glucose metabolism is impaired in AD, even at a preclinical stage, and a growing body of literature suggests that these findings may represent a primary pathogenic mechanism leading to neurodegeneration. Ketones are readily taken up by the brain and can serve as an alternative energy source for neurons and glia, hypothetically bypassing the glucose uptake deficit in AD. In this invited review we discuss the preclinical as well as clinical work aiming to increase ketones as a primary intervention in AD, including variations of the ketogenic diet, medium chain triglyceride supplementation, and newer, more experimental approaches.<\/jats:p>","DOI":"10.3233\/jad-240186","type":"journal-article","created":{"date-parts":[[2024,10,18]],"date-time":"2024-10-18T10:53:10Z","timestamp":1729248790000},"page":"S443-S453","source":"Crossref","is-referenced-by-count":8,"title":["Ketogenic Approaches for the Treatment of Alzheimer\u2019s Disease"],"prefix":"10.1177","volume":"101","author":[{"given":"Renata","family":"Gabuzyan","sequence":"first","affiliation":[{"name":"Division of Neurology and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher","family":"Lee","sequence":"additional","affiliation":[{"name":"Division of Neurology and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haakon B.","family":"Nygaard","sequence":"additional","affiliation":[{"name":"Division of Neurology and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-240186_ref1","doi-asserted-by":"crossref","first-page":"127","DOI":"10.1016\/0197-4580(80)90005-6","article-title":"Positron emission tomography in the study of aging and senile dementia","volume":"1","author":"Ferris","year":"1980","journal-title":"Neurobiol Aging"},{"key":"10.3233\/JAD-240186_ref2","doi-asserted-by":"crossref","first-page":"961","DOI":"10.1212\/WNL.33.8.961","article-title":"Alzheimer\u2019s disease: Focal cortical changes shown by positron emission tomography","volume":"33","author":"Foster","year":"1983","journal-title":"Neurology"},{"key":"10.3233\/JAD-240186_ref3","doi-asserted-by":"crossref","first-page":"843","DOI":"10.3233\/JAD-2010-091504","article-title":"Pre-clinical detection of Alzheimer\u2019s disease using FDG-PET, with or without amyloid imaging","volume":"20","author":"Mosconi","year":"2010","journal-title":"J Alzheimers Dis"},{"key":"10.3233\/JAD-240186_ref4","doi-asserted-by":"crossref","first-page":"1434","DOI":"10.1089\/ars.2011.4149","article-title":"Mitochondria and cell bioenergetics: Increasingly recognized components and a possible etiologic cause of Alzheimer\u2019s disease","volume":"16","author":"Swerdlow","year":"2012","journal-title":"Antioxid Redox Signal"},{"key":"10.3233\/JAD-240186_ref5","doi-asserted-by":"crossref","first-page":"949","DOI":"10.1152\/physrev.00062.2017","article-title":"Brain Glucose metabolism: Integration of energetics with function","volume":"99","author":"Dienel","year":"2019","journal-title":"Physiol Rev"},{"key":"10.3233\/JAD-240186_ref6","doi-asserted-by":"crossref","first-page":"1299","DOI":"10.1007\/s00424-020-02441-x","article-title":"Glucose transporters in brain in health and disease","volume":"472","author":"Koepsell","year":"2020","journal-title":"Pflugers Arch"},{"key":"10.3233\/JAD-240186_ref7","doi-asserted-by":"crossref","first-page":"506","DOI":"10.1007\/s00330-015-3834-9","article-title":"Cerebral perfusion in the predementia stages of Alzheimer\u2019s disease","volume":"26","author":"Binnewijzend","year":"2016","journal-title":"Eur Radiol"},{"key":"10.3233\/JAD-240186_ref8","doi-asserted-by":"crossref","first-page":"1977","DOI":"10.1212\/WNL.0b013e31823a0ef7","article-title":"Voxel-level comparison of arterial spin-labeled perfusion MRI and FDG-PET in Alzheimer disease","volume":"77","author":"Chen","year":"2011","journal-title":"Neurology"},{"key":"10.3233\/JAD-240186_ref9","doi-asserted-by":"crossref","first-page":"184","DOI":"10.1016\/S1474-4422(04)00683-0","article-title":"Is Alzheimer\u2019s disease a neurodegenerative or a vascular disorder? 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