Abstract
Axonopathy is a critical feature of many nervous system disorders including peripheral neuropathies and neurodegenerative diseases like ALS and Parkinson's disease. Studies of Wlds mutant mice have demonstrated that axonal degeneration is an active process. This degenerative process can be altered by manipulating neuronal bioenergetic pathways and increased expression of enzymes involved in NAD biosynthesis. Targeting of the Nmnat molecule to the cytoplasm, mitochondria, or the nucleus all result in substantial axonal protection. Axonal protection by Nmnat expression protects axons against a variety of insults including mechanical injury, microtubule disruption and mitochondrial inhibitors, and is dependent on its NAD biosynthetic activity.
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