Thiamine and benfotiamine counteract ultrasound-induced aggression, normalize AMPA receptor expression and plasticity markers, and reduce oxidative stress in mice

Gorlova, Anna; Павлов, Д. А.; Anthony, Daniel C.; Ponomarev, Eugene D.; Sambon, Margaux; Proshin, A. T.; Shafarevich, Igor; Babaevskaya, Diana; Lesсh, Klaus-Peter; Bettendorff, Lucien; Strekalova, Tatyana

doi:10.1016/j.neuropharm.2019.02.025

Cited by 35 publications

(65 citation statements)

References 101 publications

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“…In addition, FUS protein can regulate the serine‐threonine protein kinase (Ak strain transforming, Akt) and forkhead box O1 (FOXO) proteins, further elements of GSK‐3β cascade that can explain the reported changes in GSK‐3β expression in the FUS‐tg model. Moreover, paracrine secretion by stem cells of trophic factors can ameliorate decreased vascular network density in lumbar spinal cords, a recently demonstrated disease mechanism in employed here FUS‐tg mice, which is sensitive to a therapy with angiogenetic/growth factors .…”

Section: Discussionmentioning

confidence: 99%

“…Western blot analysis on spinal cord samples and quantification of protein concentration were performed as described elsewhere (; see Table S3). Relative expression of proteins was calculated in fold changes from levels of β‐tubulin as described elsewhere . The Western blot images used for quantification are presented in Figure S6 and Appendix S1.…”

Section: Methodsmentioning

confidence: 99%

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Neuro‐Cells therapy improves motor outcomes and suppresses inflammation during experimental syndrome of amyotrophic lateral sclerosis in mice

et al. 2019

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Aims:Mutations in DNA/RNA-binding factor (fused-in-sarcoma) FUS and superoxide dismutase-1 (SOD-1) cause amyotrophic lateral sclerosis (ALS). They were reproduced in SOD-1-G93A (SOD-1) and new FUS[1-359]-transgenic (FUS-tg) mice, where inflammation contributes to disease progression. The effects of standard disease therapy and anti-inflammatory treatments were investigated using these mutants. Methods: FUS-tg mice or controls received either vehicle, or standard ALS treatment riluzole (8 mg/kg/day), or anti-inflammatory drug a selective blocker of cyclooxygenase-2 celecoxib (30 mg/kg/day) for six weeks, or a single intracerebroventricular (i.c.v.) infusion of Neuro-Cells (a preparation of 1.39 × 10 6 mesenchymal and hemopoietic human stem cells, containing 5 × 10 5 of CD34 + cells), which showed antiinflammatory properties. SOD-1 mice received i.c.v.-administration of Neuro-Cells or vehicle.Results: All FUS-tg-treated animals displayed less marked reductions in weight gain, food/water intake, and motor deficits than FUS-tg-vehicle-treated mice. Neuro-Celltreated mutants had reduced muscle atrophy and lumbar motor neuron degeneration.This group but not celecoxib-FUS-tg-treated mice had ameliorated motor performance and lumbar expression of microglial activation marker, ionized calcium-binding adapter molecule-1 (Iba-1), and glycogen-synthase-kinase-3ß (GSK-3ß). The Neuro-Cells-treated-SOD-1 mice showed better motor functions than vehicle-treated-SOD-1 group. Conclusion:The neuropathology in FUS-tg mice is sensitive to standard ALS treatments and Neuro-Cells infusion. The latter improves motor outcomes in two ALS models possibly by suppressing microglial activation. | 505MUNTER ET al.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Neuro‐Cells therapy improves motor outcomes and suppresses inflammation during experimental syndrome of amyotrophic lateral sclerosis in mice

et al. 2019

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“…In animal models of amyloid plaque formation, benfotiamine reduces amyloid plaque numbers and phosphorylated tau levels, elevates the phosphorylation of glycogen synthase kinase-3α and -3β, and improves memory [31]. In other animal models, benfotiamine modulates activation of GSK3-β [32], restores neurogenesis [26,33], modulates AMPA receptor expression [25] and decreases oxidative stress [26]. Together, these results suggest that benfotiamine may be therapeutically beneficial for AD.…”

Section: Introductionmentioning

confidence: 95%

“…For example, mice [22] and humans [23] that have genetic defects in the thiamine transporter can be treated with high dose benfotiamine. Benfotiamine is an antioxidant [24][25][26], modulates arachidonic acid inflammation pathways, nuclear transcription Factor κB (NF-κβ), protein kinase B, mitogen-activated protein kinases (MAPK) and vascular endothelial growth factor receptor 2 (VEGFR2) signaling pathways [14]. Recent studies suggest that restoring cerebral perfusion by preventing neutrophil adhesion may provide another strategy for improving cognition in AD participants [27].…”

Section: Introductionmentioning

confidence: 99%

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Benfotiamine and Cognitive Decline in Alzheimer’s Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial

Gibson

Luchsinger

Cirio

et al. 2020

JAD

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Background: In preclinical models, benfotiamine efficiently ameliorates the clinical and biological pathologies that define Alzheimer’s disease (AD) including impaired cognition, amyloid-β plaques, neurofibrillary tangles, diminished glucose metabolism, oxidative stress, increased advanced glycation end products (AGE), and inflammation. Objective: To collect preliminary data on feasibility, safety, and efficacy in individuals with amnestic mild cognitive impairment (aMCI) or mild dementia due to AD in a placebo-controlled trial of benfotiamine. Methods: A twelve-month treatment with benfotiamine tested whether clinical decline would be delayed in the benfotiamine group compared to the placebo group. The primary clinical outcome was the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog). Secondary outcomes were the clinical dementia rating (CDR) score and fluorodeoxyglucose (FDG) uptake, measured with brain positron emission tomography (PET). Blood AGE were examined as an exploratory outcome. Results: Participants were treated with benfotiamine (34) or placebo (36). Benfotiamine treatment was safe. The increase in ADAS-Cog was 43% lower in the benfotiamine group than in the placebo group, indicating less cognitive decline, and this effect was nearly statistically significant (p = 0.125). Worsening in CDR was 77% lower (p = 0.034) in the benfotiamine group compared to the placebo group, and this effect was stronger in the APOE ɛ4 non-carriers. Benfotiamine significantly reduced increases in AGE (p = 0.044), and this effect was stronger in the APOE ɛ4 non-carriers. Exploratory analysis derivation of an FDG PET pattern score showed a treatment effect at one year (p = 0.002). Conclusion: Oral benfotiamine is safe and potentially efficacious in improving cognitive outcomes among persons with MCI and mild AD.

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Nutritional Interventions in Treating or Ameliorating Aggression with Dietary Regimes and Protocols

Nishijo¹,

Nishijo²,

Nishimaru³

2022

Handbook of Anger, Aggression, and Violence

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Thiamine and benfotiamine counteract ultrasound-induced aggression, normalize AMPA receptor expression and plasticity markers, and reduce oxidative stress in mice

Cited by 35 publications

References 101 publications

Neuro‐Cells therapy improves motor outcomes and suppresses inflammation during experimental syndrome of amyotrophic lateral sclerosis in mice

Neuro‐Cells therapy improves motor outcomes and suppresses inflammation during experimental syndrome of amyotrophic lateral sclerosis in mice

Benfotiamine and Cognitive Decline in Alzheimer’s Disease: Results of a Randomized Placebo-Controlled Phase IIa Clinical Trial

Nutritional Interventions in Treating or Ameliorating Aggression with Dietary Regimes and Protocols

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