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Role of Thiamine in Alzheimer's Disease

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Publisher Sage Publications
Specialty Neurology
Date 2012 Jan 6
PMID 22218733
Citations 14
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Abstract

Alzheimer's disease (AD) is the most common form of dementia in elderly individuals and is associated with progressive neurodegeneration of the human neocortex. Thiamine levels and the activity of thiamine-dependent enzymes are reduced in the brains and peripheral tissues of patients with AD. Genetic studies have provided the opportunity to determine what proteins link thiamine to AD pathology (ie, transketolase, apolipoprotein E, α-1-antitrypsin, pyruvate dehydrogenase complex, p53, glycogen synthetase kinase-3β, c-Fos gene, the Sp1 promoter gene, and the poly(ADP-ribosyl) polymerase-1 gene). We reviewed the association between histopathogenesis and neurotransmitters to understand the relationship between thiamine and AD pathology. Oral thiamine trials have been shown to improve the cognitive function of patients with AD; however, absorption of thiamine is poor in elderly individuals. In the early stage of thiamine-deficient encephalopathy (Wernicke's encephalopathy), however, parental thiamine has been used successfully. Therefore, further studies are needed to determine the benefits of using parental thiamine as a treatment for AD.

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References
1.
Zhao J, Sun X, Yu Z, Pan X, Gu F, Chen J . Exposure to pyrithiamine increases β-amyloid accumulation, Tau hyperphosphorylation, and glycogen synthase kinase-3 activity in the brain. Neurotox Res. 2010; 19(4):575-83. DOI: 10.1007/s12640-010-9204-0. View

2.
McRee R, Langlais P, Chen Y, Nalwalk J, Blumenstock F, Hough L . Increased histamine release and granulocytes within the thalamus of a rat model of Wernicke's encephalopathy. Brain Res. 2000; 858(2):227-36. DOI: 10.1016/s0006-8993(99)02309-4. View

3.
Westphalen R, Scott H, Dodd P . Synaptic vesicle transport and synaptic membrane transporter sites in excitatory amino acid nerve terminals in Alzheimer disease. J Neural Transm (Vienna). 2003; 110(9):1013-27. DOI: 10.1007/s00702-003-0012-z. View

4.
Baba A, Mitsumori K, Yamada M, Nishiyama N, Matsuki N, Ikegaya Y . Beta-amyloid prevents excitotoxicity via recruitment of glial glutamate transporters. Naunyn Schmiedebergs Arch Pharmacol. 2003; 368(3):234-8. DOI: 10.1007/s00210-003-0792-6. View

5.
Lu W, Mi R, Tang H, Liu S, Fan M, Wang L . Over-expression of c-fos mRNA in the hippocampal neurons in Alzheimer's disease. Chin Med J (Engl). 1999; 111(1):35-7. View