Effets de l’association de la Sulbutiamine à un inhibiteur de l’acétylcholinestérase dans les formes légères à modérées de la maladie d’Alzheimer

Ollat, H; Laurent, Bernard; Bakchine, Serge; Michel, Bernard; Touchon, Jacques; Dubois, Bruno

doi:10.1016/s0013-7006(07)91552-3

Cited by 14 publications

(7 citation statements)

References 13 publications

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“…At the same time the improvement of attention persisted in both groups. Activities of daily living also improved in the sulbutiamine group (Ollat H et al, 2007). …”

Section: Introductionmentioning

confidence: 94%

Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes

Gibson

Hirsch

Cirio

et al. 2013

Molecular and Cellular Neuroscience

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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.

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“…At the same time the improvement of attention persisted in both groups. Activities of daily living also improved in the sulbutiamine group (Ollat H et al, 2007). …”

Section: Introductionmentioning

confidence: 94%

Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes

Gibson

Hirsch

Cirio

et al. 2013

Molecular and Cellular Neuroscience

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“…48) NAC and sulbutiamine are relatively safe sulphur compounds which are both currently used as adjuvant therapeutic agents for several clinical conditions. 13,27) Both are also known to have cytoprotective properties such as ROS scavenging and anti-apoptotic properties in several different cell lines. 16,49) However, both in vivo and in vitro studies to support their potential use in the treatment of neurodegenerative diseases are still lacking.…”

Section: Discussionmentioning

confidence: 99%

“…27) In the multicentric, randomized and double-blind trial which evaluated the effects of the association of sulbutiamine to an anti-cholinesterasic drug showed that it can be an effective adjuvant to treatment in early stage and moderate Alzheimer's disease by anticholinesterasic drugs.…”

Section: )mentioning

confidence: 99%

Sulphur Antioxidants Inhibit Oxidative Stress Induced Retinal Ganglion Cell Death by Scavenging Reactive Oxygen Species but Influence Nuclear Factor (Erythroid-Derived 2)-Like 2 Signalling Pathway Differently

Majid

Yin

2013

Biological & Pharmaceutical Bulletin

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This study aimed to show if two different sulphur containing drugs sulbutiamine and acetylcysteine (NAC) could attenuate the effects of two different insults being serum deprivation and glutamate/buthionine sulfoximine (GB)-induced death to transformed retinal ganglion cell line (RGC-5) in culture. Cells were exposed to either 5 mm of GB for 24 h or serum deprivation for 48 h with inclusion of either NAC or sulbutiamine. Cell viability, microscopic evidence for apoptosis, caspase 3 activity, reactive oxygen species (ROS), glutathione (GSH), catalase and gluthathione-S-transferase (GST) were determined. The effects of NAC and sulbutiamine on the oxidative stress related transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf-2) levels and its dependent phase II enzyme haemeoxygenase-1 (HO-1) were carried out using Western blot and quantitative-polymerase chain reaction (PCR). NAC and sulbutiamine dose-dependently attenuated serum deprivation-induced cell death. However NAC but not sulbutiamine attenuated GB-induced cell death. NAC and sulbutiamine both independently stimulated the GSH and GST production but scavenged different types of ROS with different efficacy. Moreover only sulbutiamine stimulated catalase and significantly increased Nrf-2 and HO-1 levels. In addition, the pan caspase inhibitor, benzoylcarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk) attenuated the negative effect of serum deprivation while the necroptosis inhibitor (necrostatin-1) counteracted solely an insult of GB. The neuroprotective actions of NAC and sulbutiamine in GB or serum-deprivation insult are therefore different.Key words sulphur-antioxidant; oxidative stress; reactive oxygen species; retinal ganglion cell In a neurodegenerative disease like glaucoma, oxidative stress caused by reactive oxygen species (ROS) overproduction is thought to play an important role in causing retinal ganglion cells (RGCs) death.1) ROS over production also appears to play an important role in the pathogenesis of other progressive neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and acute syndromes of neurodegeneration, such as ischemic and hemorrhagic stroke. 2,3)One cause for an elevation of intracellular ROS is thought to stem from an elevation of extracellular glutamate. 4) Excess extracellular glutamate can affect the influx of cystine into cells so reducing the rate of intracellular glutathione (GSH) formation 4) and in the process undermining a major cellular defense mechanism to maintain homeostatic levels of ROS. Mitochondria are a major target of ROS attack and at the same time is a source for ROS production such as the superoxide anion.5) Intracellular ROS levels in healthy cells therefore exist in a balanced redox state and over production as a consequence of an underlying pathogenic state leads to breakdown of homeostasis. Importantly, excess intracellular ROS can lead to a depletion of sulphur containing thiols. 4) In addition substances such as catalase, superoxid...

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“…Despite the methodological limitations of this study, this is an important observation and opens the field for sulbutiamine use in various conditions, particularly in those characterized by an impaired intracellular and central nervous system thiamine metabolism [31,32]. Overall, sulbutiamine appears to have various potential effects, such as improvement of asthenic syndromes, modulation of the wakefulness state (in extreme high doses), enhancement of long-term memory formation, chronic postinfectious fatigue amelioration, anti-ischemic effect, psycho-behavioral inhibition in major depression, modulatory effect on glutaminergic and dopaminergic cortical transmission, improvement of diabetic polyneuropathy and psychogenic erectile dysfunction parameters, reduction of amnesic effects of drug-induced schizophrenia, modulation of Alzheimer's disease, and treatment for microsporidosis caused by the intracellular parasite Encephalitozoon intestinalis (Supplementary Table S1) [3,6,7,19,[28][29][30][33][34][35][36][37][38][39].…”

Section: Introductionmentioning

confidence: 99%

Role of the Synthetic B1 Vitamin Sulbutiamine on Health

Starling-Soares¹,

Carrera-Bastos

Bettendorff

2020

Journal of Nutrition and Metabolism

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Sulbutiamine is a thiamine derivative developed in Japan in the mid-60’s as a beriberi treatment drug. Since then, different potential applications have been described. For instance, there is some evidence that sulbutiamine can have anti-fatigue, nootropic, and antioxidant effects, which led to its use as a sport supplement (although some authors argue it is actually a masking doping strategy). Moreover, this molecule has been proposed as a possible treatment for some microsporidial infections and even for certain types of cancer. Despite these potential effects, sulbutiamine is still a relatively unknown molecule, which justifies the present review, where we discuss its history and the existing literature on its health applications. We conclude that there is a great potential for sulbutiamine use, well beyond its first described function (to increase thiamine tissue concentration). Indeed, new mechanisms of action have been found, mainly associated with its derivatives. Nevertheless, and although the research on sulbutiamine started 50 years ago, only a limited number of studies were conducted during this time frame. As so, methodological concerns need to be addressed and new studies are necessary, especially randomized controlled trials. Only then will the full potential of this versatile molecule be identified.

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Effets de l’association de la Sulbutiamine à un inhibiteur de l’acétylcholinestérase dans les formes légères à modérées de la maladie d’Alzheimer

Cited by 14 publications

References 13 publications

Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes

Abnormal thiamine-dependent processes in Alzheimer's Disease. Lessons from diabetes

Sulphur Antioxidants Inhibit Oxidative Stress Induced Retinal Ganglion Cell Death by Scavenging Reactive Oxygen Species but Influence Nuclear Factor (Erythroid-Derived 2)-Like 2 Signalling Pathway Differently

Role of the Synthetic B1 Vitamin Sulbutiamine on Health

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