A Potential Agent for Promoting Repair in Neural Network Damage and Conditions: 5-Nonyloxytryptamine (Paperback) (ISBN-13: 9798230238256)

The cell modulatory interactions of PSA-NCAM have emerged as a potential area of interest for the treatment of nervous system injuries and diseases. Enhancement of PSA- NCAM expression at injury site via viral mediated transplantation has been reported to promote axonal regeneration, migration, sensory neuron integration and Purkinje axonal sprouting after injury (Zhang et al., 2007 a, b, c). Consistent expression of PSA on astrocytes via viral mediated transfection promoted axonal extension and recruitment of corticospinal precursor cells across spinal cord injuries (El Maarouf et al., 2006). Transplantation of PSA overexpressing Schwann cells has been shown to augment the repair in both spinal cord and peripheral nerve injuries (Luo et al., 2011; Jungnickel et al., 2012). Further, alterations in PSA-NCAM expression is associated with various neurodegenerative disorders, acute or chronic stress, anxiety, depression, and temporal lobe epilepsy (reviewed by Aonurm-Helm et al., 2016). Despite of its immense therapeutic potential, availability of purified form of bacterial PSA faces major limitations for its clinical implementation. The process involves degradation of native PSA by neuraminidase and sialidase (NEU4) enzymes present in mammals (Takahashi et al., 2012) and tedious multiple steps required for its purification and isolation from biological source (Bachle et al., 2006). Recently, glycomimetics derived from either proteins or small organic compounds have emerged as potential alternative to overcome the limitations of obtaining native glycan (Podesta et al., 2014; Saini et al., 2016 a). A PSA mimicking peptide was developed by phage display screening of large libraries using PSA-specific monoclonal antibody (Torregrossa et al., 2004). In spinal cord injury, application of PSA mimicking peptides is known to promote axonal regrowth as well as cell migration and proliferation which in turn improved locomotor recovery (Marino et al., 2009; Mehanna et al., 2010).