Scott Nugent

TL;DR: It is suggested that brain hypometabolism may precede and therefore contribute to the neuropathologic cascade leading to cognitive decline in AD, and strategies to reduce the risk of AD should aim to improve insulin sensitivity by improving systemic glucose utilization, or bypass deteriorating brain glucose metabolism using approaches that safely induce mild, sustainable ketonemia.

TL;DR: The cerebral metabolic rate of glucose (CMRg) is lower in specific brain regions in Alzheimer's disease as discussed by the authors, with CMRg and Kg in the parietal cortex, posterior cingulate, and thalamus being the most affected.

TL;DR: New information is provided about glucose and ketone metabolism in the human brain and a comparison of the extent to which their regional use changes during normal aging is compared.

TL;DR: A robust and simple bias-adjustment scheme is presented for neuroimaging-based brain age frameworks and it was shown efficient and statistically improved results, making it a necessary part for future brainAge frameworks.

TL;DR: Ketones from MCT compensate for the brain glucose deficit in AD in direct proportion to the level of plasma ketones achieved.