Government declarations of war on drugs or disease often end in losing battles. That is why some neuroscientists have greeted the Obama administration’s goal of preventing or treating Alzheimer’s by 2025 with skepticism. “Setting target dates for any research program always carries the danger of falsely raising expectations,” says Kenneth S. Kosik, a professor of neuro­science at the University of California, Santa Barbara. “Research does not function like an assembly line in which we can project outcomes.” President Barack Obama signed the National Alzheimer’s Project Act into law more than a year ago, and the White House handed in a draft of the plan to Secretary of Health and Human Services Kathleen Sebelius in February. The proposal includes $50 million in new research funding for this year.

The 2025 deadline is not as unrealistic as it might seem. In war, anticipating the enemy’s next move is half the battle, and some of the most meaningful advances in Alzheimer’s research in recent years have to do with reconnaissance. Studies have shown that magnetic resonance imaging, positron-emission tomography and spinal taps—and newer methods now in the lab—can detect the effects of the buildup of aberrant proteins char­acteristic of Alzheimer’s some 10 to 15 years before the first symptoms appear. They may be able to go back further, identifying a persistent inflammatory response deep within the brain or capturing the period when mitochondria, the cellular powerhouses, begin spewing toxins as early as middle age. These are normal accompaniments of aging in all of us. For some, however, these changes interact with bad genes or other unidentified risk factors to initiate the torturously slow process that ends with dementia.

Leading research groups are already calculating what they can do with this molecular intelligence report. In February a group of researchers from Case Western Reserve University reported online in Science that a cancer drug with relatively benign side effects was able to rapidly clear from the brains of mice toxic amyloid-beta protein fragments that accompany Alzheimer’s. The compound is headed to human trials and, if it proves its mettle, could perhaps be a prelude to a statinlike drug for dementia.

For now biomarkers, as researchers call them, offer the best hope for establishing a path toward staving off cognitive decline—and for meeting the Obama administration’s ambitious goal.

This article was published in print as "The Mind Recovery Act."