Parkinson’s progress: Biogen Idec-Yale discover new pathway to disease

At the recent Society for Neuroscience Annual Meeting in Washington, DC, researchers at Biogen Idec and Yale University Medical School described a new method that may slow and possibly reverse the effects of Parkinson’s disease. Parkinson’s is one of a handful of neurodegenerative disorders that has seen a dramatic increase in prevalence as Western populations age.

Randall C Willis
CAMBRIDGE, Mass.—At the recent Society for Neuroscience Annual Meeting in Washington, DC, researchers at Biogen Idec and Yale University Medical School described a new method that may slow and possibly reverse the effects of Parkinson's disease. Parkinson's is one of a handful of neurodegenerative disorders that has seen a dramatic increase in prevalence as Western populations age.
 
According to a recent report by Kalorama Information, the market for neurotherapeutics is expected to experience double-digit growth over the next five years and possibly surpass $40 billion by 2009.
 
"This trend is driven by the tremendous advances over the past few years in understanding the genetic and molecular basis of neurodegenerative diseases, and will undoubtedly result in novel, breakthrough treatments in the next two decades," explains Dr. Alphonse Galdes, vice president of drug discovery at Biogen Idec. "It is this hope that drives our work."
 
The Biogen Idec and Yale researchers found that they could increase the levels of the neurotransmitter dopamine, necessary for smooth coordinated muscle movement, and improve behavioral response in a rodent model of Parkinson's by inhibiting the NoGo-66 receptor (NgR1).
 
"We have a multiyear collaboration with Yale to define the biology and potential therapeutic utility of the NoGo pathway," says Galdes. "We have discovered that the potential of the NoGo pathway extends well beyond spinal cord injury, and that it may provide an intervention point for the treatment of chronic neurodegenerative diseases such as Parkinson's and Alzheimer's disease."
 
Project collaborator and Yale professor of neurology Dr. Stephen Strittmatter concurs. "Axonal damage occurs in multiple sclerosis, and NgR-based treatments might promote axonal repair, but there is currently no experimental evidence published on this front," he says. That being said, Galdes states that Biogen Idec is actively pursuing research in this area.
 
If this finding translates to humans, it opens the door to therapeutics that directly target the disease rather than simply ameliorate the symptoms.
 
"Current treatments help the disease by chemically replacing the missing neurotransmitter," explains Strittmatter. "They do not slow down the ongoing loss of dopamine-containing axons and cells from the brain."
 
According to Galdes, the research on the NgR pathway is complementary to Biogen Idec's clinical studies with V2006, which is a novel drug for the symptomatic treatment of Parkinson's with potential to reduce the major side effect of current symptomatic treatments.
 
The priority for Biogen Idec now is to generate a variety of NgR1 antagonists and move the entire study further toward the clinic. Galdes indicates that the three-dimensional structure of NgR1 has been solved by Biogen Idec and others, and the data suggest that the protein belongs to a novel subgroup of the leucine-rich repeat family of proteins.
 
"We have also discovered several closely related family members, which are also involved in axonal regeneration," he adds. "Based on these data we have designed a series of protein-based antagonists of NgR, which we hope to move into the clinic in the next few years."

Randall C Willis

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