Email updates

Keep up to date with the latest news and content from BMC Neuroscience and BioMed Central.

This article is part of the supplement: Proceedings of the 8th International Conference on Alzheimer's Disease Drug Discovery

Open Access Highly Accessed Review

Hypometabolism as a therapeutic target in Alzheimer's disease

Lauren C Costantini*, Linda J Barr, Janet L Vogel and Samuel T Henderson

Author affiliations

Accera, Inc., Interlocken Crescent, Broomfield, Colorado 80021, USA

For all author emails, please log on.

Citation and License

BMC Neuroscience 2008, 9(Suppl 2):S16  doi:10.1186/1471-2202-9-S2-S16

Published: 3 December 2008

Abstract

The pathology of Alzheimer's disease (AD) is characterized by cerebral atrophy in frontal, temporal, and parietal regions, with senile plaques, dystrophic neurites, and neurofibrillar tangles within defined areas of the brain. Another characteristic of AD is regional hypometabolism in the brain. This decline in cerebral glucose metabolism occurs before pathology and symptoms manifest, continues as symptoms progress, and is more severe than that of normal aging. Ketone bodies are an efficient alternative fuel for cells that are unable to metabolize glucose or are 'starved' of glucose. AC-1202 is designed to elevate serum ketone levels safely. We previously showed that treatment with AC-1202 in patients with mild-to-moderate AD improves memory and cognition. Treatment outcomes were influenced by apolipoprotein E genotype status. These data suggest that AC-1202 may be an effective treatment for cognitive dysfunction by providing an alternative substrate for use by glucose-compromised neurons.