Modes of Action of Taurine and Granulocyte Colony-stimulating Factor in Neuroprotection

New therapeutic targets are becoming increasingly popular for the treatment of a wide array of neurodegenerative diseases, the preferred targets being those that prevent neuronal apoptosis at multiple levels or those that can cross the blood-brain barrier in order to replace degenerated cells and promote neuronal regeneration. One such rapidly emerging neuroprotective agents is taurine. Taurine is a ubiquitous amino acid that satisfies most criteria to be classified as a neurotransmitter. Because of a wide spectrum of effects that taurine can induce on intrinsic apoptosis pathways, such as modulating mitochondrial pore permeability, attenuating endoplasmic reticulum stress, maintaining calcium homeostasis, and downregulating the activities of a range of pro-apoptotic proteins, including calpain and caspases, while upregulating a variety of anti-apoptotic proteins involved in glutamate and hypoxia-induced toxicity, taurine is being extensively studied and successfully applied for the treatment of neurodegenerative diseases. Another potential molecule being researched for combating neurodegenerative diseases is granulocyte colony-stimulating factor (G-CSF), which originates from the cytokine family of growth factors. G-CSF has gained widespread attention because of its ability to cross the blood-brain barrier, the presence of its receptors in the central nervous system, anti-apoptotic functions, and its proliferative role in the restoration of tissue survival via neurogenesis. In this review from the available current literature, the modes of action of taurine and G-CSF are discussed. Further mechanistic studies are warranted in order to fully realize the potential of these two molecules.