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Molecular mechanisms in the initiation phase of Wallerian degeneration
Author(s) -
Chang Biao,
Quan Qi,
Lu Shibi,
Wang Yu,
Peng Jiang
Publication year - 2016
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13250
Subject(s) - wallerian degeneration , nicotinamide mononucleotide , degeneration (medical) , neuroscience , axon , axonal degeneration , biology , microbiology and biotechnology , neurodegeneration , nicotinamide adenine dinucleotide , nad+ kinase , biochemistry , medicine , pathology , enzyme , disease
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.