ArticleBMC neuroscience2026
Taurine reverses long-term memory deficits caused by LPS induced neuroinflammation.
Article in BMC neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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9 authors.
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Abstract
backgroundDespite neuroinflammation being an initially protective response made by the central nervous system (CNS), as it becomes chronic, it can lead to neuronal damage since the cytokines which are released by microglia potentialize cellular death due to excitotoxicity, and this, in turn, promotes the release of pro-inflammatory mediators, feeding this way a self-sustaining cycle of neuroinflammatory response, which favor subsequent neurodegeneration. Given the fact that until this moment, there are not any therapeutic alternatives able to stop the neurodegeneration, the objective of the present work was to evaluate the putative neuroprotector effect of taurine, a partial glycinergic ionotropic receptor agonist, and also a GABA
methodFor this intent, the oral taurine administration was evaluated on mnemonic impairing caused by LPS induced neuroinflammation in male Wistar rats. Such effects were investigated on recent and late spatial long-term memory and aversive memory in the behavioural tasks Morris water maze (MWM) and context fear conditioning (CFC), respectively. In addition, we investigated the effect of orally administered taurine on hippocampal neuronal density and on hippocampal levels of TNF-α and IL-4.
resultsTaurine, when orally administered for 30 days, in the doses of 20 and 200 mg/kg, was able to reverse the mnemonic impairment caused by neuroinflammation on recent and remote spatial long-term memory, and in the dose of 200 mg/kg, it also was able to do the same on aversive long-term memory. In the doses of 20 and 200 mg/kg, taurine was also able to reverse the LPS-induced increase in hippocampal TNF-α levels.
conclusionTaurine, when orally administered in a pathological context characterized by neuroinflammatory background, as it was induced in this work, can perform a dose-dependent neuroprotective effect, probably by acting in an excitotoxic scenario in which the activation of hyperpolarizing receptors can be welcomed.
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