Oral benfotiamine reverts cognitive deficit and increase thiamine diphosphate levels in the brain of a rat model of neurodegeneration

@article{Moraes2020OralBR,
  title={Oral benfotiamine reverts cognitive deficit and increase thiamine diphosphate levels in the brain of a rat model of neurodegeneration},
  author={Ruan Carlos Mac{\^e}do de Moraes and Monique P. Singulani and {\'A}lisson de Carvalho Gonçalves and Guilherme Vannucchi Portari and Andr{\'e}a S. Torr{\~a}o},
  journal={Experimental Gerontology},
  year={2020},
  volume={141}
}
It is well known that patients with Alzheimer's disease (AD) have imbalances in blood thiamine concentrations and lower activity of thiamine-dependent enzymes. Benfotiamine, a more bioavailable thiamine analog, has been proposed as an alternative to counteract these changes related to thiamine metabolism. Thus, our study aimed to analyze the effects of benfotiamine supplementation on brain thiamine absorption, as well as on parameters related to neuronal energy metabolism and disease… Expand
5 Citations
Neuroprotective Effects of Thiamine and Precursors with Higher Bioavailability: Focus on Benfotiamine and Dibenzoylthiamine
TLDR
In vitro studies show that another thiamine thioester, dibenzoylthiamine (DBT) is even more efficient that BFT, especially with respect to its anti-inflammatory potency. Expand
The impact of thiamine deficiency and benfotiamine treatment on Nod-like receptor protein-3 inflammasome in microglia
TLDR
Correcting thiamine metabolism through benfotiamine provides a new therapeutic strategy for NLRP3 inflammasome related neurological, metabolic, and inflammatory diseases. Expand
Mitochondrial dysfunction in Alzheimer's disease: Therapeutic implications of lithium
TLDR
A comprehensive investigation of the significance of mitochondrial dysfunction in AD and pharmacological treatment with lithium as imperative in this pathology is performed, through a brief review of the major findings on the effects of lithium as a therapeutic approach targeting mitochondria in the context of AD. Expand
Neuroinflammation in neurological disorders: pharmacotherapeutic targets from bench to bedside.
TLDR
The present review focuses on elaborating the recent advancement in understanding molecular mechanisms of neuroinflammation and its role in the etiopathogenesis of various neurological disorders, especially Alzheimer's disease, Parkinson's disease (PD), and Epilepsy. Expand

References

SHOWING 1-10 OF 60 REFERENCES
Benfotiamine treatment activates the Nrf2/ARE pathway and is neuroprotective in a transgenic mouse model of tauopathy
TLDR
Findings demonstrate that BFT activates the Nrf2/ARE pathway and is a promising therapeutic agent for the treatment of diseases with tau pathology, such as AD, frontotemporal dementia and progressive supranuclear palsy. Expand
Vitamin B1 (thiamine) and dementia
TLDR
It is shown that in preclinical models, reduced thiamine can drive AD‐like abnormalities, including memory deficits, neuritic plaques, and hyperphosphorylation of tau, and excessThiamine diminishesAD‐like pathologies. Expand
Alterations of thiamine phosphorylation and of thiamine-dependent enzymes in Alzheimer's disease
There is a growing body of evidence to suggest that thiamine neurochemistry is disrupted in Alzheimer's Disease (AD). Studies in autopsied brain tissue from neuropathologically proven AD patientsExpand
Anandamide Effects in a Streptozotocin-Induced Alzheimer’s Disease-Like Sporadic Dementia in Rats
TLDR
It is shown, for the first time, that the administration of an endocannabinoid can prevent AD-like effects induced by STZ, boosting further investigations about the modulation of endOCannabinoid levels as a therapeutic approach for AD. Expand
Thiamine and benfotiamine improve cognition and ameliorate GSK-3β-associated stress-induced behaviours in mice
TLDR
Thiamine and benfotiamine may modulate GSK‐3&bgr; functions in a manner that is dependent on whether the contextual conditioning is adaptive or maladaptive, and have antidepressant/anti‐stress effects in naïve animals that are associated with reduced GSK-3& bgr; expression and conditioning of adverse memories. Expand
Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes
TLDR
If so, the use of benfotiamine could provide a safe intervention to reverse biological and clinical processes of AD progression, and related mechanisms may lead to reversal of plaque formation by benfutiamine in animals. Expand
Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels
TLDR
It is demonstrated, for the first time, that thiamine and benfotiamine prevent stress‐induced inhibition of hippocampal neurogenesis and accompanying physiological changes, and might be useful as a complementary therapy in several neuropsychiatric disorders. Expand
Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse model
TLDR
The induction of mild impairment of oxidative metabolism, oxidative stress and inflammation induced by TD alters metabolism of APP and/or Abeta and promotes accumulation of plaques independent of neuron loss or neuritic clusters. Expand
High thiamine diphosphate level as a protective factor for Alzheimer’s disease
TLDR
Blood TDP levels were significantly decreased in female AD patients compared to male AD patients, and its protective efficacy may be independent of other metabolic factors. Expand
Powerful beneficial effects of benfotiamine on cognitive impairment and beta-amyloid deposition in amyloid precursor protein/presenilin-1 transgenic mice.
TLDR
In the animal Alzheimer's disease model, benfotiamine appears to improve the cognitive function and reduce amyloid deposition via thiamine-independent mechanisms, which are likely to include the suppression of glycogen synthase kinase-3 activities. Expand
...
1
2
3
4
5
...