Dietary supplementation with medium-chain TAG has long-lasting cognition-enhancing effects in aged dogs

Abstract

The present study focused on the hypothesis that dietary supplementation with medium-chain TAG (MCT) will improve cognitive function in aged dogs by providing the brain with energy in the form of ketones. Aged Beagle dogs were subjected to a baseline battery of cognitive tests, which were used to establish cognitively equivalent control or treatment groups. The dogs in the treatment group were maintained on a diet supplemented with 5·5 % MCT. After an initial wash-in period, all the dogs were tested with a battery of cognitive test protocols, which assessed sequentially landmark discrimination learning ability, egocentric visuospatial function and attention. The groups were maintained on the diets for 8 months. The MCT-supplemented group showed significantly better performance in most of the test protocols than the control group. The group differences also varied as a function of task difficulty, with the more difficult task showing greater supplementation effects than the easier tasks. The group given the MCT supplement showed significantly elevated levels of b-hydroxybutyrate, a ketone body. These results indicate, first, that long-term supplementation with MCT can have cognition-improving effects, and second, that MCT supplementation increases circulating levels of ketones. The results support the hypothesis that brain function of aged dogs can be improved by MCT supplementation, which provides the brain with an alternative energy source.Brain ageing: Cognitive functions: Dogs: Medium-chain TAG: Ketone bodies Dog cognitive function, like that of other mammals, becomes impaired over the course of ageing, and it provides a model of human cognitive ageing (1,2) . Decline in energy metabolism is a common feature of ageing in animals, and it is one of the several processes that are closely associated with age-dependent cognitive decline. Rapoport et al. (3) found that brain glucose metabolism was reduced by up to 30 % between 3 and 12 months of age in rats. London et al. (4) reported that brain glucose metabolism was significantly reduced in Beagle dogs at 6 years of age than in 1-year-old dogs. Further changes occurred later in life, but in a manner that varied between brain structures. Brain metabolic decline has also been reported in aged monkeys (5) and human subjects (6) , and it appears to be particularly more pronounced in pathological ageing. Alexander et al.(7) reported that cerebral glucose metabolism was significantly lower in old patients with Alzheimer's disease than in healthy old control subjects. Drzezga et al.(8) traced the development of cognitive decline in patients with mild cognitive impairment, discovering that the clinical symptoms of Alzheimer's disease were associated with further declines in cerebral glucose metabolism. These data suggest that the age-associated reduction in cerebral glucose metabolism is a common feature in ageing, that the process involved may be progressive, starting around the middle age, and that metabolic decline contributes to cognitive decline associated with ...

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