Tors with respect to that of non-demented control patients [38]. Keeping the need for identifying the indirect candidates involved besides the direct ones for in-depth exploration of the molecular networks of the disease, we transfected AICD in mouse and human neuroblastoma cell lines and identified differential expressions of proteins belonging to diverse molecular pathways [39], for example, ER-stress (GRP78), structural remodeling (vimentin) and general stress (HSP90, HSPA8).for a period of weeks after an injury, grossly the pathophysiology of SCI is divided into primary and secondary injuries. The initial trauma to the spinal cord is called primary injury and it is a prognostic indicator of SCI [46]. Following the primary injury, secondary injury sets in [47] and may last from months to D(+)-Galactosamine (hydrochloride) years. This phase witnesses a plethora of degenerative phenotypes attributed to multitudes of molecular responses to injury [48]. Therefore, in spinal cord injury research, it is very important to get a clear picture of the molecular anatomy at the PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/15501003 vicinity of the injury. On the other hand, for the peripheral nerve injuries, which comprise a greater subset of neuronal injuries, study of molecular parameters promoting axonal regeneration is of paramount importance [49]. Axon forms an important tissue to analyse changes following an injury. This is because of a temporal sequence of three events promoting neuron regeneration: discharge of axonal potentials induced by injury, interrupted normal supply of retrogradely transported targetderived factors, and retrograde injury signals travelling from the injury site back to the cell body, also called positive injury signals [50]. Here, the necessity of biomarker analysis is born. Especially, proteomics approaches are preferred to those of genomics in the domain of axonal regeneration and degeneration because changes in axons often occur without any transcriptional events in the cell body, following a pathological condition [5]. Moreover, a large number of PTMs to proteins accompany axonal degeneration and regeneration, which has been rightfully termed as a `postgenomics' problem. A series of elegant work from the group of Perlson et al., beginning with proteomics approach, showed that vimentin is translated at the site of axonal injury [51], it is retrogradely transported from the site of injury to the cell body on dynein motor [52] and binds with ERK preventing its dephosphorylation [53].Clinical proteomics in spinal cord injury Acute traumatic injury of the spinal cord resulting in partial or total deficits in sensory and/or motor functions is widely prevalent worldwide and leads to considerable decline in the quality of life [40]. Though relative annual incidences of SCI vary with the geographical region and the time period of the study [41], studies show that global average incidence is highest in Asia [40] with 43.8 persons per million people afflicted. Traffic accidents [42], fall from height [43] and violence [44] constitute some of the major reasons for SCI. Autonomic dysfunctions that follow SCI set the major decline in the quality of life of afflicted persons. An injury above the C3 level in the vertebral column may lead to immediate cardiac arrest necessitating assisted respiration [45]. While the autonomic deregulations may lastClinical proteomics tools to discover molecular interplay post SCI Application of proteomics in biomarker analysis in traumatic SCI has found inflammatory cytokines at el.