Alcohol, Ageing and Cognitive FunctionA nutritional perspective
Jenny Svanberg, Adrienne Withall, Brian Draper, Stephen Bowden in Alcohol and the Adult Brain, 2014
Thiamine is a water-soluble vitamin occurring in free or phosphorylated forms in most plant and animal tissues. Lipid-soluble precursors of thiamine have a higher bioavailability than the basic thiamine molecule. Benfotiamine (s-benzoylthiamine) has been found to prevent the progression of diabetes, but does not alter brain levels of thiamine. More effective lipid-soluble compounds, such as allithiamine and synthetic sulbutiamine and fursultiamine, do increase levels of brain thiamine (Volvert et al., 2008).
Micronutrients in Prevention and Improvement of the Standard Therapy in Diabetes
Kedar N. Prasad in Micronutrients in Health and Disease, 2019
Diabetes can lead to thiamine deficiency. Treatment of streptozotocin-induced diabetic mice with benfotiamine, a lipophilic derivative of thiamine, reduced cerebral oxidative stress without affecting the levels of advanced glycation end-product (AGE), protein carbonyl, tissue factor, and TNF-alpha.189 These results suggest that the primary action of benfotiamine is mediated via antioxidation.
Thiamine alleviates cognitive impairment and epileptogenesis by relieving brain inflammation in PTZ-induced kindling rat model
Published in Neurological Research, 2022
Sebahattin Karabulut, Ahmet Kemal Filiz, Recep Akkaya
It suggests that inflammation and seizures contribute to neuropsychiatric comorbidities of epilepsy [42]. Moreover, cognitive impairments such as spatial memory deficit frequently manifest in patients with epilepsy [43]. Consistent with our results, it has been shown in previous studies that PTZ-induced epileptogenesis causes learning and memory impairments [44,45]. Chemical kindling induced by PTZ leads to structural pathological changes, oxidative stress, and neuroinflammation in the hippocampus, which is the essential structure of the brain in learning and memory [46,47]. Our results showed that thiamine pretreatment alleviated learning deficits caused by PTZ-kindling. A recent experimental study showed that oral benfotiamine supplementation increased thiamine diphosphate concentrations in the hippocampus and entorhinal cortex, and it improved the STZ-related cognitive deficit in rats [48]. Evidence indicates that thiamine is a neuroinflammation modulator known for removing reactive oxidative species [12,49]. Also, previous studies reported that benfotiamine can exert antiinflammatory effects [50,51]. Considering the constantly increasing oxidative stress and inflammation in the epileptic hippocampus, it is plausible that the neuroprotective effect of thiamine is likely a result of its potent anti-inflammatory effect.
Pharmacotherapeutic options for co-morbid depression and alcohol dependence
Published in Expert Opinion on Pharmacotherapy, 2019
Thomas Hillemacher, Helge Frieling
Chronic alcoholism is frequently associated with significant nutritional and vitamin deficiencies, including vitamin B1 (thiamine) deficiency that is associated with depression and other psychiatric disorders [102]. Approximately 30–80% of inpatients admitted for alcohol treatment are thiamine deficient [102]. Benfotiamine, a synthetic S-acyl thiamine derivative, significantly ameliorates mitochondrial dysfunction and attenuates oxidative damage and inflammation [103]. Manzardo et al. evaluated the efficacy of the benfotiamine in a 6-month randomized, double-blind, placebo-controlled clinical pilot trial [102]. They randomized 85 male patients with current DSM-IV diagnoses of alcohol dependence with or without depressive symptoms on benfotiamine (600 mg/d) or placebo. The results suggested that thiamine deficiency contributes significantly to psychiatric distress in severe AUD supporting the possible benefit of thiamine supplementation for the alleviation of depressive symptomatology in patients with AUD. This can be considered an adjuvant therapy in alcohol rehabilitation [102].
High thiamine diphosphate level as a protective factor for Alzheimer’s disease
Published in Neurological Research, 2018
Changpeng Wang, Guoqiang Fei, Xiaoli Pan, Shaoming Sang, Lijun Wang, Chunjiu Zhong, Lirong Jin
Moreover, blood TDP level is a potential protective factor for cognition in non-demented older adults [22], which is consistent with the OR value of 0.95 we obtained when TDP levels were treated as continuous variables. To date, four clinical trials using thiamine or thiamine derivatives for AD treatment have been conducted, and conflicting results were reported [36–39]. In addition to the small sample sizes, another reasonable explanation for the divergent results is that the hydrophilic compound thiamine is poorly absorbed by older adults [19,40]. Based on a longitudinal study of 5 mild or moderate AD patients, benfotiamine 300 mg/d administered orally for as long as 18 months appeared to improve cognitive function by an average of 3.2 points as assessed by the MMSE [35]. Thus, TDP, an active form of thiamine, may be a potential target for AD disease-modifying therapy. Recently, two independent phase II clinical trials evaluating the protective efficacy of benfotiamine for AD are under way (ClinicalTrials.gov, identifier: NCT02292238; Chinese Clinical Trial Registry, Registration number: ChiCTR1800014316). The results are coming in 2 years.
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