Drug Development Overview

Background

Abnormal glucose metabolism in Alzheimer’s Disease (AD) is linked to cognitive issues. This is similar to what happens with a lack of thiamine (vitamin B1) in the brain. In animal studies, thiamine deficiency leads to memory loss, neuron damage, brain inflammation, and other AD-like symptoms. Increasing thiamine levels significantly using benfotiamine can reduce these issues.

Study Findings

A pilot trial lasting 12 months tested benfotiamine on patients with mild AD. Key results include:

Blood thiamine levels increased over 100 times compared to placebo.
43% less decline in cognitive function (ADAS cog).
77% less worsening of cognitive decline (CDR).
Benfotiamine reduced elevated advanced glycation end products (AGE).

Methodology

The study analyzed blood samples from patients to identify changes in metabolites and lipids after treatment with benfotiamine.

Results

Researchers identified:

315 unique metabolites and 417 lipids.
25 metabolites and 22 lipid species changed positively after benfotiamine treatment.
Significant changes were noted in glucose metabolism and aromatic amino acid production.

Conclusion

Benfotiamine appears to reverse metabolic changes related to AD. Further research is ongoing to validate these findings and explore the use of metabolic biomarkers for diagnosing and monitoring AD. This research is funded by the National Institute of Aging.