• Cover story

    • Low-Rhes approach to Huntington's

      by Tim Fulmer, Senior Writer

      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.