Impact of Exercise and Vitamin B&lt;sub&gt;1&lt;/sub&gt; Intake on Hippocampal Brain-Derived Neurotrophic Factor and Spatial Memory Performance in a Rat Model of Stress

Dief, Abeer E.; Samy, Doaa M.; Dowedar, Fatma I

doi:10.3177/jnsv.61.1

Cited by 30 publications

(27 citation statements)

References 32 publications

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“…We considered the possibility that thiamine and/or benfotiamine might exert protective effects on AHN when mice are exposed to stressful events. Recently, the involvement of thiamine-dependent protective mechanisms in stress response was reported in forced swim and immobilization stress models (Dief et al, 2015). However, the effects of increased thiamine levels on neuroplasticity during stress response were not addressed and no data on the effects of thiamine or benfotiamine on brain neurogenesis have been available.…”

Section: Introductionmentioning

confidence: 99%

Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels

Vignisse

Sambon

Gorlova

et al. 2017

Molecular and Cellular Neuroscience

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Thiamine is essential for normal brain function and its deficiency causes metabolic impairment, specific lesions, oxidative damage and reduced adult hippocampal neurogenesis (AHN). Thiamine precursors with increased bioavailability, especially benfotiamine, exert neuroprotective effects not only for thiamine deficiency (TD), but also in mouse models of neurodegeneration. As it is known that AHN is impaired by stress in rodents, we exposed C57BL6/J mice to predator stress for 5 consecutive nights and studied the proliferation (number of Ki67-positive cells) and survival (number of BrdU-positive cells) of newborn immature neurons in the subgranular zone of the dentate gyrus. In stressed mice, the number of Ki67- and BrdU-positive cells was reduced compared to non-stressed animals. This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3β (GSK-3β) upregulation in the CNS. Moreover, we show that thiamine and benfotiamine counteract stress-induced bodyweight loss and suppress stress-induced anxiety-like behavior. Both treatments induced a modest increase in the brain content of free thiamine while the level of thiamine diphosphate (ThDP) remained unchanged, suggesting that the beneficial effects observed are not linked to the role of this coenzyme in energy metabolism. Predator stress increased hippocampal protein carbonylation, an indicator of oxidative stress. This effect was antagonized by both thiamine and benfotiamine. Moreover, using cultured mouse neuroblastoma cells, we show that in particular benfotiamine protects against paraquat-induced oxidative stress. We therefore hypothesize that thiamine compounds may act by boosting anti-oxidant cellular defenses, by a mechanism that still remains to be unveiled. Our study demonstrates, for the first time, that thiamine and benfotiamine prevent stress-induced inhibition of hippocampal neurogenesis and accompanying physiological changes. The present data suggest that thiamine precursors with high bioavailability might be useful as a complementary therapy in several neuropsychiatric disorders.

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Section: Introductionmentioning

confidence: 99%

Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels

Vignisse

Sambon

Gorlova

et al. 2017

Molecular and Cellular Neuroscience

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“…Patients with TD neuropathy were observed with limited locomotion [ 45 , 46 ]. In a rat model of stress, thiamine supplementation was shown to increase the locomotor activity of stressed rats by regulating the brain-derived neurotrophic factor and acetylcholine in the hippocampus [ 47 ]. Adult male Swiss mice, when treated with thiamine antagonist pyrithiamine in conjunction with a TD diet, showed a reduction in locomotor activity during the course of dietary treatment [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

“…Thiamine is used to treat patients with anxiety, and it was shown to improve many of the symptoms, suggesting an anxiolytic effect of thiamine [ 59 , 60 ]. Thiamine supplementation ameliorated the anxiety-like behavior of stressed-induced rats [ 47 ] and stress-induced mice [ 61 ]. TD causes symptoms including fatigue, anorexia, and nausea, which are also observed in anxiety disorders.…”

Section: Discussionmentioning

confidence: 99%

Thiamine Deficiency Causes Long-Lasting Neurobehavioral Deficits in Mice

Wen

et al. 2020

Brain Sciences

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Thiamine deficiency (TD) has detrimental effects on brain health and neurobehavioral development, and it is associated with many aging-related neurological disorders. To facilitate TD-related neuropsychological studies, we generated a TD mouse model by feeding a thiamine-deficient diet for 30 days, followed by re-feeding the control diet for either one week or 16 weeks as recovery treatment. We then performed neurobehavioral tests in these two cohorts: cohort of one week post TD treatment (1 wk-PTDT) and 16 weeks post TD treatment (16 wks-PTDT). The TD mice showed no significant difference from control in any tests in the 1 wk-PTDT cohort at the age of 13–14 weeks. The tests for the 16 wks-PTDT cohort at the age of 28–29 weeks, however, demonstrated anxiety and reduced locomotion in TD animals in open field and elevated plus maze. In comparison, rotor rod and water maze revealed no differences between TD and control mice. The current findings of the differential effects of the same TD treatment on locomotion and anxiety at different ages may reflect the progressive and moderate change of TD-induced neurobehavioral effects. The study suggests that, even though the immediate neurobehavioral impact of TD is modest or negligible at a young age, the impact could develop and become severe during the aging process.

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“…On a biochemical level, exercise has been shown to reverse some of the neurological changes induced by exposure to psychosocial and/or physical stressors, including release of hippocampal corticosterone, decreased neurogenesis, and impaired hippocampal-dependent behaviors, such as learning and memory (227–230). In animal models of stress, both forced and voluntary exercise interventions have been shown to restore neuronal differentiation in the hippocampus (231, 232), increase levels of hippocampal brain-derived neurotrophic factor (BDNF) (233–235), and restore cognitive function (233, 236). There is also evidence that exercise-induced neurochemical changes, including increased production of hippocampal BDNF and altered hippocampal glucocorticoid receptor levels, may be protective against the stress response (237–239).…”

Section: Lifestyle Modification and Dietary Supplementsmentioning

confidence: 99%

Impacts of Psychological Stress on Osteoporosis: Clinical Implications and Treatment Interactions

et al. 2019

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The significant biochemical and physiological effects of psychological stress are beginning to be recognized as exacerbating common diseases, including osteoporosis. This review discusses the current evidence for psychological stress-associated mental health disorders as risk factors for osteoporosis, the mechanisms that may link these conditions, and potential implications for treatment. Traditional, alternative, and adjunctive therapies are discussed. This review is not intended to provide therapeutic recommendations, but, rather, the goal of this review is to delineate potential interactions of psychological stress and osteoporosis and to highlight potential multi-system implications of pharmacological interventions. Review of the current literature identifies several potentially overlapping mechanistic pathways that may be of interest (e.g., glucocorticoid signaling, insulin-like growth factor signaling, serotonin signaling) for further basic and clinical research. Current literature also supports the potential for cross-effects of therapeutics for osteoporosis and mental health disorders. While studies examining a direct link between osteoporosis and chronic psychological stress are limited, the studies reviewed herein suggest that a multi-factorial, personalized approach should be considered for improved patient outcomes in populations experiencing psychological stress, particularly those at high-risk for development of osteoporosis.

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Impact of Exercise and Vitamin B<sub>1</sub> Intake on Hippocampal Brain-Derived Neurotrophic Factor and Spatial Memory Performance in a Rat Model of Stress

Cited by 30 publications

References 32 publications

Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels

Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels

Thiamine Deficiency Causes Long-Lasting Neurobehavioral Deficits in Mice

Impacts of Psychological Stress on Osteoporosis: Clinical Implications and Treatment Interactions

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