Despite major advances in early diagnosis, neuroimaging, and biomarker research, no dis-ease-modifying therapies are available for Alzheimer's Disease (AD). Reduced glucose me-tabolism is an invariant feature of AD and is an outstanding biomarker of disease progres-sion. Vitamin B1 deficiency reduces glucose metabolism and causes serve memory deficits in animals and humans. Vitamin B1 administration reverses both abnormalities. In animals, vitamin B1 deficiency increases plaques and tangles, which are characteristic features of AD. Further, administration of vitamin B1 to mice to mice that have plaques and tangles diminishes plaques, tangles and memory deficits. Vitamin B1 dependent processes are diminished in brains from AD patients. This pilot study will test whether increasing vitamin B1 will be beneficial in patients with AD. The proposed tests will use clinical outcome and reversal of a biomarker, brain glucose utilization, as endpoints. The risk to the patients is minimal, and the potential benefit large.