Vitamin B1 (thiamine) and dementia

Gary E. Gibson, Joseph A. Hirsch, Pasquale Fonzetti, Barry D. Jordan, Rosanna T. Cirio, Jessica Elder

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

The earliest and perhaps best example of an interaction between nutrition and dementia is related to thiamine (vitamin B1). Throughout the last century, research showed that thiamine deficiency is associated with neurological problems, including cognitive deficits and encephalopathy. Multiple similarities exist between classical thiamine deficiency and Alzheimer's disease (AD) in that both are associated with cognitive deficits and reductions in brain glucose metabolism. Thiamine-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients and by thiamine decline, and a decrease in their levels could account for the reduction in glucose metabolism. In preclinical models, reduced thiamine can drive AD-like abnormalities, including memory deficits, neuritic plaques, and hyperphosphorylation of tau. Furthermore, excess thiamine diminishes AD-like pathologies. In addition to dietary deficits, drugs or other manipulations that interfere with thiamine absorption can cause thiamine deficiency. Elucidating the reasons why the brains of AD patients are functionally thiamine deficient and determining the effects of thiamine restoration may provide critical information to help treat patients with AD.

Original languageEnglish (US)
Pages (from-to)21-30
Number of pages10
JournalAnnals of the New York Academy of Sciences
Volume1367
Issue number1
DOIs
StatePublished - Mar 1 2016

Keywords

  • Alzheimer's disease
  • Glucose metabolism
  • Mitochondria
  • Thiamine
  • Vitamin B1

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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