Molecular mechanisms in the initiation phase of Wallerian degeneration.
Axonal degeneration is an early hallmark of nerve injury and many neurodegenerative diseases. The discovery of the Wallerian degeneration slow mutant mouse, in which axonal degeneration is delayed, revealed that Wallerian degeneration is an active progress and thereby illuminated the mechanisms underlying axonal degeneration. Nicotinamide mononucleotide adenylyltransferase 2 and sterile alpha and armadillo motif-containing protein 1 play essential roles in the maintenance of axon integrity by regulating the level of nicotinamide adenine dinucleotide, which seems to be the key molecule involved in the maintenance of axonal health. However, the function of nicotinamide mononucleotide remains debatable, and we discuss two apparently conflicting roles of nicotinamide mononucleotide in Wallerian degeneration. In this article, we focus on the roles of these molecules in the initiation phase of Wallerian degeneration to improve our understanding of the mechanisms underpinning this phenomenon.
['Chang|Biao|B|', 'Quan|Qi|Q|', 'Lu|Shibi|S|', 'Wang|Yu|Y|', 'Peng|Jiang|J|']
D000818:Animals D001369:Axons D006801:Humans D009243:NAD D009419:Nerve Tissue Proteins D019636:Neurodegenerative Diseases D009474:Neurons D014855:Wallerian Degeneration
nicotinamide mononucleotide nicotinamide mononucleotide adenylyltransferase 2 sterile alpha and armadillo motif-containing protein 1 nicotinamide adenine dinucleotide