When it comes to prognosis, the mouse models I use to study amyotrophic lateral sclerosis (ALS) are sadly accurate – like their human counterparts with familial ALS, all mice with these mutations die young. After 20 years of trying – and failing – to find a treatment that could extend life, I was close to giving up, until a new drug candidate came along. Then something amazing happened – a mouse lived.
Joe Beckman |
Every day I receive emails from ALS patients and their loved ones, which is both gratifying and heart breaking. The time from onset of the disease to death can be just a few years, and patients are desperate for some hope. The possibility that my work might help these people is a large part of what has kept me going for over 20 years, despite all the setbacks and frustrations.
My ALS journey actually started with an interest in oxidative stress. I was studying the oxidant peroxynitrite, which mediates tyrosine nitration – a process you can find in stroke, diabetes, heart disease, neurodegenerative disorders and many other conditions. One of the major antioxidant defenses that prevents the formation of peroxynitrite and protects the body from oxidative stress is the protein superoxide dismutase (SOD). But SOD also has a dark side – we discovered that it can catalyze tyrosine nitration, speeding up oxidative damage.
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