Vitamin B1 (thiamine) and dementia

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 deficiency, and their decline could account for the reduction in glucose metabolism. In preclinical models, reduced thiamine can drive AD-like abnormalities, including memory deficits, 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.

Enhanced Activities of Blood Thiamine Diphosphatase and Monophosphatase in Alzheimer's Disease

“…Decreased TDP levels and thiamine-dependent enzymes activities were found in AD patients but not in patients with vascular dementia, frontotemporal dementia and Parkinson’s disease[9,16]. Our previous study demonstrated that thiamine metabolism can serve as a promising biomarker for AD diagnosis with high sensitivity and specificity over 80%[8].…”

“…Both TDP level[8,9,10,11] and activities of TDP-dependent enzymes[12,13,14,15] have been demonstrated to be significantly decreased in AD. Previous studies have demonstrated that thiamine deficiency can induce or aggravate AD-like pathologies, such as neuritic plaques, and hyperphosphorylation of tau, finally memory deficits[16]. Furthermore, benfotiamine supplementary, a lipid-soluble thiamine derivative, diminished AD-like pathologies and cognitive function in AD animal models[17].…”

The Catalytic Mechanism of Human Transketolase

“…[1,2] Since hTK substrates and products are intermediates of other fundamental metabolic processes, such as glycolysis and the glucuronic acid pathway, [3] its activity is strictly related to treatment and prevention of various diseases. [8,9] In the case of brain dysfunctions [10] and diabetes mellitus, [11,12] regular hTK's activity has been monitored and related to prevention of these diseases. [4,5] Additionally, tumor cells growth has been blocked by inhibiting non-oxidative phase of PPP in which hTK is involved [6,7] and, moreover, the reduced activities of hTK have been linked to diseases affecting brain tissues, such as Alzheimer's disease.…”

Validation of a HPLC Method for Quantification of Thiamine and Its Phosphate Esters in Rat Brain Tissue

“…Symptoms observed in WKS include oculomotor disturbance, ataxia and confusion (acute symptoms), and amnesia and confabulation (chronic symptoms) [9] [10]. Rodent models of TD have been developed to examine the pathogenesis of these disorders [11].…”