ALS, Alzheimer's Insights Could Improve Treatment

"This might well be a therapeutic opportunity," Bruijn said. "The finding in these rodents is that you can slow the progression of the disease. But it's a big leap into the clinic," she cautioned.

"ALS patients are desperate for a therapy," Bruijn noted. "We have to be cautious; this is a laboratory study. It's a promise, it's a hope that might be meaningful if there are careful steps to translate it to humans."

In the second report, researchers led by Dr. Lennart Mucke, director, senior investigator and a professor of neurology and neuroscience at the Gladstone Institute of Neurological Disease in San Francisco, found that changing the metabolism of fatty acids could slow cognitive decline in mice afflicted with Alzheimer's.

"We discovered that an enzyme that clips off certain fatty acids from lipids in the brain seems to be activated by poisonous proteins [amyloid proteins] that build up in the brains of Alzheimer patients," Mucke said. "These fatty acids can do a lot of damage and impair memory."

In their experiments, Mucke's team noted that in mice with Alzheimer's, there was an increase in omega-6 fatty acid, known as arachidonic acid, and also its metabolic byproduct. This process is also involved in the production of amyloid-beta peptide, which is linked to the plaques and tangles in the brain that are a hallmark of the disease.

When the researchers blocked the activation of the arachidonic acid-metabolizing enzyme, they found that the mice had significant improvements in some learning and memory tasks.

"We were able to improve memory deficits and improve other behavioral abnormalities in these Alzheimer models," Mucke said. "This suggests that there may be a new therapeutic path where one could use inhibitors of this enzyme to prevent the release of detrimental fatty acids in the brain."

Since the researchers were able to prevent the progression of memory deficits, their next step is to see if they can reverse memory damage that has already occurred, Mucke said.

Dr. Samuel Gandy, Mount Sinai Professor of Alzheimer's Disease Research at the Mount Sinai School of Medicine in New York City and chairman emeritus of the National Medical and Scientific Advisory Council of the Alzheimer's Association, was less optimistic.

"It's an interesting new strategy," Gandy said. But since other methods of reversing amyloid-beta plaques have failed in human clinical trials, he wondered whether this latest attempt to do so will translate to a real benefit for patients.

"In general, making and curing mouse models of amyloid-beta toxicity has turned out to be relatively easy, but none of the 'mouse cures' have had any meaningful impact on human Alzheimer's disease," Gandy said.

More information

For more about neurological disease, visit the National Institute of Neurological Disorders and Stroke.

SOURCES: Lennart Mucke, director, senior investigator, professor, neurology and neuroscience, Gladstone Institute of Neurological Disease, San Francisco; Nicholas Maragakis, M.D., neurologist/researcher, Johns Hopkins University School of Medicine, Baltimore; Lucie Bruijn, M.D., science director, senior vice president, ALS Association; Samuel Gandy. M.D., Ph.D., professor, Alzheimer's Disease Research, Mount Sinai School of Medicine, New York City, chairman emeritus, National Medical and Scientific Advisory Council, Alzheimer's Association; Oct. 19, 2008,Nature Neuroscience, online