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Posted September 24, 2012: by Bill Sardi
Comment: without a proven cure for Alzheimer’s disease, clinicians should move vitamin B1 (thiamin) to their “A” list of potential remedies. Coffee, tea, alcohol, sugar, all block B1 absorption. Fat-soluble B1 (benfotiamine) was developed for this very purpose. Accompanying signs of B1 deficiency would be nystagmus (lateral eye twitches), chronic diarrhea, fibromyalgia-like symptoms, heart failure, greying of hair, diabetic complications in eyes and kidneys. — Bill Sardi, Knowledge of Health, Inc.
Mol Cell Neurosci. 2012 Sep 13. pii: S1044-7431(12)00177-7. doi: 10.1016/j.mcn.2012.09.001. [Epub ahead of print]
Department of Neurology and Neuroscience, Weill Cornell Medical College, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605. Electronic address: email@example.com.
Reduced glucose metabolism is an invariant feature of Alzheimer’s Disease (AD) and an outstanding biomarker of disease progression. Glucose metabolism may be an attractive therapeutic target, whether the decline initiates AD pathophysiology or is a critical component of a cascade. The cause of cerebral regional glucose hypometabolism remains unclear. Thiamine-dependent processes are critical in glucose metabolism and are diminished in brains of AD patients at autopsy. Further, the reductions in thiamine-dependent processes are highly correlated to the decline in clinical dementia rating scales. In animal models, thiamine deficiency exacerbates plaque formation, promotes phosphorylation of tau and impairs memory. In contrast, treatment of mouse models of AD with the thiamine derivative benfotiamine diminishes plaques, decreases phosphorylation of tau and reverses memory deficits. Diabetes predisposes to AD, which suggests they may share some common mechanisms. Benfotiamine diminishes peripheral neuropathy in diabetic humans and animals. In diabetes, benfotiamine induces key thiamine- dependent enzymes of the pentose shunt to reduce accumulation of toxic metabolites including advanced glycation end products (AGE). Related mechanisms may lead to reversal of plaque formation by benfotiamine in animals. If so, the use of benfotiamine could provide a safe intervention to reverse biological and clinical processes of AD progression. This article is part of a Special Issue entitled ‘Mitochondrial function’.
Copyright © 2012. Published by Elsevier Inc.
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