This is the authors' abstract. We don't add key points for this paper.
Evidence linking abnormalities in thiamine (vitamin B1) availability and metabolism to the pathophysiology of Alzheimer's Disease (AD) has focused attention on the regulation of thiamine as a therapeutic target.A recently completed pilot clinical trial in AD patients revealed that increasing blood thiamine to pharmacologically high levels using benfotiamine has potential efficacy in treating persons with early AD.These results support the underlying hypothesis that thiamine insufficiency promotes AD and is a druggable target.A mechanistic understanding of thiamine's cellular actions and improved methods to deliver thiamine to the brain are fundamental to optimize the use thiamine homeostasis as a target of engagement.Benfotiamine has a therapeutic product profile in AD that includes raising blood thiamine to pharmacologically high levels, with excellent safety and potential for clinical efficacy.It is a potentially widely available treatment.
Answers are grounded in this paper and cite their sources.
No takes yet. Share an insight, caveat, or question.
Gibson et al. (2022) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: