Fig. 1.

Schematic diagram of the deleterious effects of oxidative damage in Huntington’s disease neurons. Under stress, MT release high levels of ROS, which can act at short distance as radicals and as peroxide at longer distance. The MT are the source and major target of oxidation. The activated ROS interacts with DNA, RNA, cell membranes, and cytoplasmic proteins, as examples. Additionally, damaged MT eventually diminish their ATP production leading to energy depletion and cell death in the HD neurons. This mechanism may apply to other neurodegenerative diseases as well.