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http://www.alsa.org/research/grants.cfm?grant_id=171&type_id=&category_id=&state=&country=&title="&institution=&investigator=190&zip=&radius=250&action=detailJuly 12, 2007
The ALS Association Announces 2007 Research Funding:
New Efforts Promise Accelerated Progress
Roberta Friedman, Ph.D., Research Department Information Coordinator
The ALS Association announces new projects that build on the most recent progress in understanding the disease process in order to devise effective treatment. Proposals include several approaches to find ALS biomarkers, molecules that specifically can report the onset, presence, and progression of the disorder to speed diagnosis, increase efficiency of clinical trials, and provide focused targets for developing new, effective therapies.
The grants awarded include funding to researchers around the world. The ALS Association currently funds more than 20 international grants in more than 12 different countries. The criteria for funding are based on innovative, cutting-edge science regardless of the country in which it is produced. In some cases, studies abroad offer unique opportunities. This is the case with stem cell research as legal requirements to conduct this research vary widely from country to country. For genetics studies, some countries may offer particular population characteristics or cultural and socioeconomic factors. Ireland for instance provides a relatively homogeneous population with health information maintained in databases enabled by socialized medicine, a situation that is particularly useful for looking at likely risk factors for ALS.
Funding Begins August 1, 2007
Although motor neurons are the cells that die in ALS, the cells that surround them are not innocent bystanders. Agar and his team will use a state-of-the-art technique that harnesses a highly focused laser to the technique called mass spectroscopy, a way to measure precisely the molecular composition of the motor neurons that might change in the disease. This project will be funded by the Alan L. Phillips Discovery Grant Award made possible through support from Morton and Malvina Charlestein.
Chaudhuri in collaboration with John Hart will use precise methods to find which proteins are changed in the disease in order to identify potential biomarkers. Blood samples reflecting the gene activity in ALS patients might be able to provide biomarkers, a possibility to be pursued by van den Berg and Ophoff, using genome-wide analysis with the most up-to-date gene finding technology. Borchelt and Shaw are poised to follow up encouraging findings pointing to the ability of a protein in nerve fibers to serve as an ALS biomarker. Wiedau-Pazos and Karsten will seek genes that are differently active in mice with one or the other of two different mutations that can produce ALS, using gene finder chips.
The Tanguay lab in collaboration with Jean-Pierre Julien, Ph.D., will see if symptoms are changed in mice that make more than the usual amount of certain helper molecules, the heat shock proteins. These mice will also make the mutant protein, copper-zinc superoxide dismutase (SOD1), linked to some inherited forms of ALS. They are choosing in particular those helper molecules that are specific to the mitochondria, the cell power plants that show damage in ALS. Barrett and colleagues will follow up on observations about the way nerve endings attempt self repair in SOD1 mutant mice challenged by conditions that mimic intense exercise, a risk factor suspect in the disease. Siddique and Deng will see if over producing the protective SOD enzyme, SOD2, can help with mutant SOD1 toxicity.
In research directed at the issue of why SOD1 mutations produce ALS, Beckman proposes to test further his idea that loss of zinc from this altered protein explains the toxicity.
Progress in using stem cells to model the disease will be translated by the Zhang lab to determine interactions among motor neurons and their neighbors that produce the damage in ALS and to find out why the most common mutation to the SOD1 protein in people does not produce appreciable symptoms in mice. Macklis and collaborators seek to extend findings suggesting that stem cells in the brain might be stimulated to repair damage in ALS. His focus is on the motor neurons reaching from the brain to the spinal cord, one of the few investigations focusing on this aspect of ALS. Maragakis will see if the supportive cells called glia can be generated from stem cells to aid repair in a mouse model of ALS.
Xu proposes to create a mouse with another mutation linked to the disease in order to provide greater insight into the complexity of the disease process and find the common reason why motor neurons die. Lansbury and Ray have made progress in finding compounds that can potentially protect against the toxic properties of mutant SOD1 protein and propose to further refine their leads to come up with a testable drug candidate.
Please access The ALS Association Active Research Projects Searchable Database throughout the year to see currently funded grants. |
