Taurine (TAU) reaches a high concentration in the central nervous system
(CNS). The physiological role of TAU in the CNS is the subject of many
investigations. It has been suggested that this amino acid could act as a membrane
stabilizer, a modulator of calcium signaling, a trophic factor for neuronal development,
and even be proposed as a neurotransmitter in the CNS. Besides, several investigations
revealed the neuroprotective properties of TAU in various experimental models.
Multiple mechanisms, including the inhibition of the excitotoxic response, the blockade
of cytoplasmic calcium overload, regulation of oxidative stress, and the positive effects
of TAU on mitochondrial parameters, have been proposed for the neuroprotective
properties of this amino acid. Today, it is well-known that mitochondrial function and
energy metabolism play a pivotal role in the pathogenesis of various neurodegenerative
disorders and xenobiotics-induced neurotoxicity. Hence, targeting mitochondria with
safe and clinically applicable agents is a viable therapeutic option in various
neurodegenerative disorders. In the current chapter, the effects of TAU on the CNS will
be highlighted, focusing on the positive effects of this amino acid on mitochondrial
parameters. The data could help the development of safe therapeutic agents against
CNS complications.
Keywords: Brain injury, Energy crisis, Mitochondrial dysfunction, Neurodegenerative disease, Neurotoxicity, Oxidative stress.
