By activating GABA and glycine receptors, taurine inhibits excitotoxicity caused by Aβ-induced glutamatergic transmission activation 22. Anti-inflammatory and anti-oxidant properties of taurine also protect neuronal cells and mitochondria from neurotoxicity of Aβ. The electron microscopy study indicates that taurine weakly inhibits Aβ aggregation 21. During the development of AD, amyloid-β (Aβ) progressively misfolds into toxic aggregates, which are strongly associated with neuronal loss, synaptic damages and brain atrophy. Taurine also has multiple disease-modifying roles to prevent or cease neuropathology of AD. Notably, taurine does not enhance learning and memory in cognitively intact adult rodents 20. In streptozotocin-induced sporadic dementia rat models, cognitive impairment and abnormal acetylcholinesterase activity is ameliorated by taurine 19. Taurine supplementation has also been found to rescue ageing-dependent loss of visual discrimination in mice 18. In addition, intravenously administered taurine significantly improves post-injury functional impairments of traumatic brain injury in rats 17. The intracerebroventricular administration of taurine protects mice from hypoxia-induced learning impairment 16. Cognitive deficits of rats from excess manganese exposure are improved and upregulated acetylcholinesterase activity is partially restored after taurine administration 15. Taurine recovers memory impairments of mice induced by alcohol, pentobarbital, sodium nitrite and cycloheximide without any observable effects on other behaviours including motor coordination, exploratory activity and locomotor activity 14. Recently, taurine has shown therapeutic effects as a cognitive enhancer in animal models of non-AD neurological disorders. Due to its nontoxic and curative properties, taurine is frequently found in food, drinks and drugs for treating liver and heart disorders 10, 11, 12, 13. Taurine, 2-aminoethanesulfonic acid, is the second most abundant endogenous amino acid in the central nervous system (CNS) and plays multiple roles in our body: thermoregulation, stabilization of protein folding, anti-inflammatory effects, antioxidation, osmoregulation, calcium homeostasis and CNS development 3, 4, 5, 6, 7, 8, 9 ( Figure 1). However, the unnecessary stimulation of the normal cholinergic systems in the brains of AD patients and, even, non-demented subjects remains to be solved 2. The next generation acetylcholinesterase inhibitors may well fit into the accelerated pathways. Albeit flexible in mechanisms of action, these symptomatic drugs must be assessed in early-stage AD patients with overt dementia and apparent biomarkers, such as amyloid plaques and tau tangles. Their new guidance suggests accelerated regulatory pathways for drugs that improve cognitive deficits alone in early stages of AD. Accordingly, the US Food and Drug Administration loosened the standard for AD drug approval 1. This has become evident after consecutive failures in clinical trials for disease-modifying drugs that target neuropathological hallmarks. Recovery from dementia is the key clinical benefit to the patients of Alzheimer's disease (AD). While the exact mechanism of taurine in AD has not yet been ascertained, our results suggest that taurine can aid cognitive impairment and may inhibit Aβ-related damages. In the cortex of APP/PS1 mice, taurine slightly decreased insoluble fraction of Aβ. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice. We orally administered taurine via drinking water to adult APP/PS1 transgenic mouse model for 6 weeks. In this study, we assessed cognitively enhancing property of taurine in transgenic mouse model of AD. It has demonstrated neuroprotective properties against many forms of dementia. Our study focuses on taurine, an endogenous amino acid found in high concentrations in humans. Recently, US Food and Drug Administration mitigated the standard for drug approval, allowing symptomatic drugs that only improve cognitive deficits to be allowed to accelerate on to clinical trials. Alzheimer's disease (AD) is a lethal progressive neurological disorder affecting the memory.
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