Rust and Neurodegeneration

Rust and Neurodegeneration

"Reactive Oxygen Species led to axonal degeneration"

Reactive Oxygen Species Promote Axon Degeneration
Craig Press and Jeffrey Milbrandt

Several neurodegenerative diseases, like Parkinson’s disease (PD), are
linked to mitochondrial dysfunction, which decreases ATP production
and increases reactive oxygen species (ROS). Likewise, disrupting
mitochondrial function can cause neurodegeneration; for example, the
pesticide rotenone, which inhibits mitochondrial electron transport,
produces PD-like symptoms in animals and causes axonal degeneration in
cultured dorsal root ganglion (DRG) neurons. Press and Milbrandt now
report that expression of nicotinamide mononucleotide
adenylyltransferase (Nmnat) in DRG neurons slows rotenone-induced
axonal degeneration. The protective effects of Nmnat were likely due
to reduced accumulation of ROS, since Nmnat had little effect on ATP
levels in the neurons. Furthermore, other treatments that increased
ROS led to axonal degeneration, treatments that reduced ROS prevented
degeneration, and long-term depletion of ATP produced no sign of
degeneration. The results support the hypothesis that ROS accumulation
is involved in many neurodegenerative processes, including those
related to mitochondrial dysfunction.

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