Cover story
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Low-Rhes approach to Huntington's
June 25 2009, Volume 2 / Number 25
Johns Hopkins researchers may have solved a central mystery of Huntington's disease: why the mutant form of the huntingtin protein occurs throughout the body and yet causes pathology primarily in the brain. The proposed target, Rhes, also looks to be druggable.
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Analysis
Science for export
Although every major university or institute would like to be located in a biotech hub and keep its discoveries close to home, only a few true hubs exist. For everyone else, the question is whether their research will be taken elsewhere for commercialization. In the long run, the answer is usually yes.
Seeing CNV sooner
A multinational research team suggests that noninvasive imaging of CCR3 could help detect incipient wet age-related macular degeneration, making earlier therapeutic intervention possible. The researchers also suggest that CCR3 inhibition could be used to augment treatment with VEGF-A inhibitors.
Proteasome progress
Researchers at Proteolix have found a small molecule that inhibits a subunit of the proteasome involved in immune cell activation. The compound's profile could make it suitable for autoimmune indications, an area previously off-limits to general proteasome inhibitors because of toxicity concerns.
