Numerous evidences suggest the prevalence of axonal degeneration (AxD) prior to onset of many neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease and amyotrophic lateral sclerosis. Wallerian degeneration (WD) is an anciently noted pattern of AxD that follows injury or chemical insult. At molecular level, WD is regulated by the action of a novel protein called sterile alpha and Toll/interleukin receptor (TIR) motif-containing 1 (SARM1). SARM1 contains an ARM domain, two tandem SAM domains and a TIR domain. Previous structural and functional data revealed the NADase activity of TIR domain, which is facilitated by the octameric SAM domain. Loss of NAD+ due to activation of SARM1 is the main culprit in AxD. Recent structural data showed how ARM domain disintegrates TIR self-interaction and thus, maintains autoinhibition. The ARM domain can interact with both NAD+ and NMN, a precursor of NAD+. These two molecules play a crucial role as the molecular switch of SARM1. This mechanism is conserved through different organisms; however, quite elusive so far. To understand the whole pathway, it is essential to determine the active conformation of SARM1. This project aims to solve the 3D structure of the activated protein and to understand how the catalytic activity is regulated at molecular level.