Abstract
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.
Highlights
Thiamine is an essential vitamin required for normal growth and tissue development
To determine the effects of TD on behavioral tests, two cohorts of animals were used in this study: cohort of one week post thiamine deficiency treatment (1 wk-PTDT cohort) and cohort of 16 weeks post thiamine deficiency treatment (16 wks-PTDT cohort)
The average body weights of each group in both cohorts were similar at the beginning of the experiments, and there was no significant difference (F(3, 35) = 0.5779, p = 0.6334): control of 1 wk-PTDT = 26.3 ± 0.4 g; TD of 1 wk-PTDT = 25.7 ± 0.5 g; control of 16 wks-PTDT = 25.9 ± 0.4 g; TD of 16 wks-PTDT = 26.5 ± 0.5 g
Summary
Thiamine is an essential vitamin required for normal growth and tissue development. It cannot be synthesized by the human body; it needs to be supplied in food or as a dietary supplement.The activated form of thiamine, thiamine pyrophosphate or diphosphate (TPP), serves as a cofactor for several key enzymes involved in carbohydrate metabolism. Thiamine is an essential vitamin required for normal growth and tissue development. It cannot be synthesized by the human body; it needs to be supplied in food or as a dietary supplement. There are many factors that may cause thiamine deficiency (TD): insufficient dietary intake, consumption of anti-thiamine factors, excessive loss of vitamin B1, and chronic alcohol consumption [1,2,3]. TD was shown to cause mild and chronic impairment of oxidative metabolism, neuroinflammation, and neurodegeneration, which are the processes commonly observed in Wernicke–Korsakoff syndrome (WKS) and many aging-related neurodegenerative diseases such as Alzheimer’s disease [9], Parkinson’s disease [10], and progressive supranuclear palsy [11]. Animal models for TD are useful for research of WKS and aging-associated degenerative disorders
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