Chronic treatment with sulbutiamine improves memory in an object recognition task and reduces some amnesic effects of dizocilpine in a spatial delayed-non-match-to-sample task

Bizot, Jean-Charles; Herpin, Alexandre; Pothion, Stéphanie; Pirot, Sylvain; Trovero, Fabrice; Ollat, H

doi:10.1016/j.pnpbp.2005.04.035

Cited by 16 publications

(11 citation statements)

References 25 publications

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“…Chronic administration of sulbutiamine improves long-term memory formation in mice (Micheau et al, 1985). Chronic treatment with sulbutiamine improves memory in an object recognition task and reduces some amnesic effects of dizocilpine in a spatial delayed-non-match-to-sample task (Bizot et al, 2005). …”

Section: Introductionmentioning

confidence: 99%

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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Section: Introductionmentioning

confidence: 99%

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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“…The kind of memory that is assessed in ORT is different in motive and content; PAT evaluates the implicit memory while ORT assesses explicit memory [43,44]. In PAT, rodents learn to avoid an aversive stimulus (electric foot-shock) by inhibiting a response, so it is related to an aversive memory while ORT shows non-aversive spatial memory [42,45]. Second, different parts of the brain might be involved in these two tests.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Citicoline and Benfotiamine Each Alone and in Combination on Streptozotocin-induced Memory Impairment in Mice

Safavi

Hosseini-Sharifabad

Seyed-Yousefi

et al. 2020

Clin Psychopharmacol Neurosci

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Objective: Diabetes mellitus is associated with cognitive disorders such as Alzheimer's disease. Studies have shown that citicoline and benfotiamine can improve memory and learning through different mechanism of actions. The aim of this study was to compare the individual effects of benfotiamine (100, 200, 300 mg/kg) and citicoline (50, 100, 250, 500 mg/kg, gavage) and their co-administration on memory impairments in diabetic mice. Methods: Diabetes was induced by a single dose of streptozotocin (STZ, 140 mg/kg, intraperitoneal) and benfotiamine and/or citicoline were administered for three weeks. Memory was evaluated using the object recognition task (ORT) and passive avoidance test (PAT). Results: Results from ORT shows that citicoline at 50, 100, 250, and 500 mg/kg and benfotiamine at 100, 200, and 300 mg/kg and their combination (benfotiamine at 100 mg/kg added to citicoline at 50, 100, and 250 mg/kg) are equally effective in reversing the memory loss induced by STZ (p ＜ 0.001). PAT results demonstrate that citicoline at 100, 250, and 500 mg/kg and benfotiamine at above doses did not improve the latency time when administered separately, but benfotiamine at a fixed dose of 100 mg/kg in the presence of citicoline at 50, 100, and 250 mg/kg increased the latency time and improved memory significantly. Conclusion: In conclusion, in PAT, co-administration of benfotiamine and citicoline was more effective than either alone in improving memory. Regarding ORT, although benfotiamine added to citicoline improved memory notably, the difference between combination therapy and single-drug therapy was not considerable.

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“…Sulbutiamine is a vitamin B1 derivative which has the ability of crossing blood brain barrier due to its lipophilic nature 2 . It is used in the treatment of cognitive disorder and memory dysfunction due to decrease in the cholinergic activity [3][4][5] .…”

Section: Introductionmentioning

confidence: 99%

Development and Validation of Stability Indicating Spectrophotometric Methods for Determination of Sulbutiamine in Tablet Dosage Form

Lotfy

Abdallah

Al‐Ghobashy

2016

Analytical Chemistry Letters

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Five sensitive, selective and precise stability-indicating spectrophotometric methods for the determination of Sulbutiamine (SUL) in the presence of its alkali-induced degradation product (DEG) were developed and validated. Method A is differential dual wavelength (D 1 DWL) applied in the analysis of SUL in binary mixture via its first derivative spectra using the difference between two points with equal amplitudes in the alkali-induced degradation product, thus DEG acts as zero contribution. Method B is second derivative spectrophotometry (D 2 ), which allowed the determination of SUL at 300.0 nm. Method C is second derivative of the ratio spectra (DD 2 ) in which SUL was determined by measuring the peak amplitude at 301.0 nm. Method D is the ratio difference spectrophotometry (RD), where the difference between amplitudes of the absorbance ratio spectra at 237.2 and 274.0 nm were recorded and Method E; Ratio subtraction (RSM) where the zero order spectra of pure SUL were extracted from their laboratory prepared mixtures, and consequently SUL can be analyzed at its maxima. The linearity for SUL was obtained within concentrations ranging from 5.00 -50.00 μg/mL with percentage recovery of 100.58 + 0.98, 99.62 ± 1.16, 100.70 ± 1.38, 100.06 + 1.00 and 99.56 + 1.00 for the five methods, respectively. IntroductionSulbutiamine(SUL)[4-[(4-amino-2-methylpyrimidin-5-yl)methyl-formyl-amino]-3-[2-[(4-mino-2-methyl-pyrimidin-5-yl)methyl-formylamino]-5-(2-methylpropanoyloxy)pent-2-en-3-l] disulfanyl-pent-3-enyl]2-methylpropanoate ( Fig. 1) 1 . Sulbutiamine is a vitamin B1 derivative which has the ability of crossing blood brain barrier due to its lipophilic nature 2 . It is used in the treatment of cognitive disorder and memory dysfunction due to decrease in the cholinergic activity 3-5 .

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Chronic treatment with sulbutiamine improves memory in an object recognition task and reduces some amnesic effects of dizocilpine in a spatial delayed-non-match-to-sample task

Cited by 16 publications

References 25 publications

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

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

Protective Effects of Citicoline and Benfotiamine Each Alone and in Combination on Streptozotocin-induced Memory Impairment in Mice

Development and Validation of Stability Indicating Spectrophotometric Methods for Determination of Sulbutiamine in Tablet Dosage Form

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