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Preventive effects of taurine against d-galactose-induced cognitive dysfunction and brain damage
Dom-Gene Tu1, Yao-Ling Chang, Chung-Hsi Chou
1Department of Nuclear Medicine, Ditmanson Medical Foundation, Chia-Yi Christian Hospital, Chia-Yi City 600, Taiwan.
Abstract:
Oxidative stress arising from life processes or environmental influences and its resultant cellular dysfunctions are major causes of neurodegenerative disorders. The objectives of this study were to investigate whether taurine (Tau) can prevent d-galactose-induced cognitive dysfunction and brain oxidative damage. Mice given with Tau supplementation (100 and 400 mg per kg BW per day) spent shorter (p < 0.05) time in searching target in d-galactose (100 mg per kg BW per day) treated mice in a water maze reference memory experiment. Moreover, Tau supplementation extended (p < 0.05) the searching period around the target quadrant in the probe test of the water maze, and neuronal degeneration and nucleus shrinkage in the hippocampus dentate gyrus area of d-galactose treated mice were observed to be attenuated. Tau also downregulated (p < 0.05) expression of the glial fibrillary acidic protein (Gfap) and of the cluster of differentiation marker Cd11b; meanwhile, it strengthened (p < 0.05) antioxidant capacity and lowered (p < 0.05) the accumulation of advanced glycation end-products (AGEs) in the brain. Therefore, Tau could be effective to ameliorate oxidative damage and inflammation in the brain, and apoptosis of brain cells, which further lessen the cognitive dysfunction.
Insights
Taurine (Tau) supplementation improved cognitive function and reduced brain oxidative damage in mice. This suggests taurine may be effective in preventing neurodegeneration and cognitive decline.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Neurodegenerative disorders are often linked to oxidative stress and cellular dysfunction.
- d-galactose exposure can induce cognitive deficits and oxidative brain damage.
Purpose of the Study:
- To investigate the neuroprotective effects of taurine (Tau) against d-galactose-induced cognitive impairment and oxidative stress in mice.
- To evaluate taurine's impact on brain antioxidant capacity and inflammation markers.
Main Methods:
- Mice were treated with d-galactose and varying doses of taurine (100 and 400 mg/kg BW/day).
- Cognitive function was assessed using a water maze reference memory experiment.
- Brain tissue analysis examined neuronal integrity, glial fibrillary acidic protein (Gfap), cluster of differentiation marker Cd11b, and advanced glycation end-products (AGEs).
Main Results:
- Taurine supplementation significantly improved performance in the water maze, indicating enhanced memory.
- Neuronal degeneration and nucleus shrinkage in the hippocampus were attenuated by taurine.
- Taurine downregulated Gfap and Cd11b expression, indicating reduced inflammation, and increased antioxidant capacity while lowering AGEs.
Conclusions:
- Taurine effectively ameliorates d-galactose-induced cognitive dysfunction and brain oxidative damage.
- Taurine demonstrates potential in reducing brain inflammation and apoptosis, offering neuroprotection.
- Taurine supplementation is a promising strategy for mitigating neurodegenerative processes associated with oxidative stress.
