Induction of ketosis may improve mitochondrial function and decrease steady-state amyloid-β precursor protein (APP) levels in the aged dog

Dietary Enrichment with Medium Chain Triglycerides (AC-1203) Elevates Polyunsaturated Fatty Acids in the Parietal Cortex of Aged Dogs: Implications for Treating Age-Related Cognitive Decline

“…The present study did not utilize a ketogenic diet, and protein and carbohydrate levels were maintained at adequate levels. However, as previously reported, higher rates of fatty acid oxidation were achieved by exogenously adding MCT to the normal chow diet [17]. This is because, in contrast to longer chain fatty acids ([12 carbons), MCT undergo obligate hepatic oxidation.…”

“…Under conditions of enhanced fatty acid oxidation or ketosis, polyunsaturated fatty acids are preferentially mobilized from adipose tissue or liver, to other tissues, including the brain [16]. AC-1203 has been shown to increase fatty acid oxidation in aged dogs [17]. Thus, the rise in brain PUFA concentrations in the MCT-treated group is likely due to a metabolic effect of the AC-1203 on fatty acid oxidation and subsequent redistribution of PUFA from adipose tissue and liver to the brain.…”

Nutrition of Aging Dogs

“…In another study, mediumchain triglyceride-supplemented dogs demonstrated improved mitochondrial function, redox status, and fewer amyloid protein deposits. 32 Further, supplementation with medium-chain triglycerides resulted in improved cognitive performance in old dogs, compared with unsupplemented controls. 83 Nutritional Intervention for Declining Immunity Many aging changes occur as a result of oxidative damage at a cellular and subcellular level.…”

The Expanding Role of Ketogenic Diets in Adult Neurological Disorders

“…In vitro studies showed attenuation of deleterious amyloid-β induced effects on rat cortical neurons by pre-treatment with coconut oil (containing high concentrations of MCT) or medium chain fatty acids via activation of Akt and extracellular-signal-regulated kinase (ERK) signaling pathways [104]. Similarly, preclinical studies using animal models of dementia demonstrated reduced brain amyloid-β levels, protection from amyloid-β toxicity and better mitochondrial function following administration of the KD, ketones and MCT [105,106,107,108]. Importantly, ketone body suppression of mitochondrial amyloid entry has been further shown to improve learning and memory ability in a symptomatic mouse model of AD [109].…”