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Neuronal injuries such as stroke, traumatic brain injury, and spinal cord injury are leading causes of major disability and death. Chronic therapy for these neuronal injuries requires the promotion of axonal regeneration from the remaining neurons (Schwab and Strittmatter, 2014). However, the local environment in the central nervous system (CNS) is unfavorable to this regeneration due to the presence of myelin-derived axonal growth inhibitors such as Nogo-A, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp). In addition, chondroitin sulfate proteoglycans (CSPGs) associated with astroglial scarring also inhibit axonal regeneration after neuronal injury. Several studies support the role of Nogo-A in limiting axonal regeneration. It has two distinct domains with antineuritogenic potential: N-terminal amino-Nogo and C-terminal Nogo-66, a 66 amino acid containing domain. Strittmatter and his associates identified a cell surface glycosyl phosphatidylinositol-anchored membrane protein, NgR1, as a receptor for Nogo-66 (Schwab and Strittmatter, 2014). Later studies have revealed that MAG, OMgp, and CSPGs also bind to NgR1 which may mediate their inhibiting activity on the axonal growth. NgR1 signals through interaction with p75 neurotrophin receptor (p75NTR) or a homologous protein, TROY, as well as a transmembrane protein, LINGO-1. The association between p75NTR and Rho-GDI leads to the release of RhoA and its activation. RhoA in turn activates its effector, Rho-associated protein kinase (ROCK). This ultimately leads to actin-cytoskeletal reorganization, which results in the collapse of growth cones and inhibition of neurite outgrowth (Figure 1).

Counteraction of Nogo-A and axonal growth inhibitors by green tea polyphenols and other natural products