Links To And Excerpts From “Supplemental thiamine as a practical, potential way to prevent Alzheimer’s disease from commencing”

In this post, I link to and excerpt from Supplemental thiamine as a practical, potential way to prevent Alzheimer’s disease from commencing [PubMed Abstract] [Full-Text] [Full-Text PDF]. Alzheimers Dement (N Y). 2021 Jul 28;7(1):e12199.

Similar articles for PMID: 34337137 – 79 Results

All that follows is from the above resource.


Can one thiamine tablet a day keep Alzheimer’s away? This article argues that it may do so. The multiple elements that contribute to pathogenesis of Alzheimer’s dementia include mitochondrial depression, increased ROS, lactic acidosis and cerebral acidosis of the brain, cerebral depositions of amyloid and tau, synaptic dysfunction, disturbed neurotransmission, cognitive impairments, and disturbances affecting astrocytes, endothelial cells, and the blood brain barrier. Most of those elements of Alzheimer’s pathogenesis are addressed by thiamine which, if used at a time when a middle‐aged person still has normal cognition, may prevent those components of pathogenesis from developing. In brief: it is easier to prevent Alzheimer’s than to try to reverse it after it has developed. The data supporting the prophylactic use of thiamine are robust. In order to validate its use, a clinical trial is advocated that would enroll persons aged 65 or older who have evidence of depositions of amyloid or tau in their brains, and randomly assign them to take, for as long as 5 years, either thiamine 100 mgs daily or a matched placebo tablet.


It is better to attempt stopping Alzheimer’s disease (AD) before it starts than trying to cure it after it has developed. A cerebral scan showing deposition of either amyloid or tau identifies those elderly persons whose cognition is currently normal but who are at risk of subsequent cognitive loss that may develop into AD. Synaptic hypometabolism is usually present in such at‐risk persons. Although inadequate adenosine triphosphate (ATP) may cause synaptic hypometabolism, that may not be the entire cause because, in fact, measurements in some of the at‐risk persons have shown normal ATP levels. Thiamine deficiency is often seen in elderly, ambulatory persons in whom thiamine levels correlate with Mini‐Mental State Examination scores. Thiamine deficiency has many consequences including hypometabolism, mitochondrial depression, oxidative stress, lactic acidosis and cerebral acidosis, amyloid deposition, tau deposition, synaptic dysfunction and abnormal neuro‐transmission, astrocyte function, and blood brain barrier integrity, all of which are features of AD. Although the clinical benefits of administering supplementary thiamine to patients with AD or mild cognitive impairment have been mixed, it is more likely to succeed at preventing the onset of cognitive loss if administered at an earlier time, when the number of aberrant biochemical pathways is far fewer. Providing a thiamine supplement to elderly persons who still have normal cognition but who have deposition of either amyloid or tau, may prevent subsequent cognitive loss and eventual dementia. A clinical trial is needed to validate that possibility.

Keywords: Alzheimer’s, cognitive loss, commencement, early, prevent, thiamine
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