In the study of Alzheimer's disease, the smallest steps forward have sometimes led to the most exciting breakthroughs.

In the case of a recent study from Novato's Buck Institute, it's a molecular step forward -- specifically, modifying a single amino acid in the brains of lab mice that could prevent the frightening memory loss and dementia associated with Alzheimer's disease.

While several scientists outside the Buck Institute were reluctant to call the study a true breakthrough, the results "are not a trivial step forward," said Stephen Snyder, an Alzheimer's disease specialist with the National Institute on Aging.

"This opens the door on a field of research. What these guys are showing, basically, is a new universe for us to look into more deeply," Snyder said. "We don't know much about the mechanisms. You could fault these people for rushing to print the study without knowing that, but in the Alzheimer's field, we accept a lot of this because these little incremental things could mean a lot."

Alzheimer's is a debilitating neurological disease that affects 4.5 million Americans, and with the Baby Boomer generation a decade or so away from the at-risk years, scientists have been under increasing pressure to develop treatments for the disease.

There are dozens, even hundreds, of studies being conducted on Alzheimer's at any given time, as scientists reconsider 15-year-old theories that haven't yet led to viable treatments, or spin off into new, untapped realms of brain chemistry research.

In the Buck Institute study, a protein was altered in the brains of lab mice. The mice that received the treatment showed all the pathological signs of suffering Alzheimer's disease -- most notably, a buildup of sticky plaque that scientists believe is related to the disease -- but had none of the memory-loss symptoms or brain shrinkage.

It's too soon to say whether the genetic alteration that seems to have worked on mice will also work on humans, but the research shines new light on the progression of Alzheimer's disease, said Dale Bredesen, chief executive of the Buck Institute.

"It gives you a completely different view of a disease you thought you understood. It points us in the direction of a new way to treat it," Bredesen said. "Because you cure the mouse, can you cure the human? Time will tell. But since we do have such a big impact on the mouse, it does lead us to new treatments options."

The next step for scientists is further research on the genetic alteration and, ultimately, drug therapy for humans, Bredesen said. A drug treatment is at least two years away, he said, and on average it takes 14 years for a drug to get FDA approval.

Several scientists not affiliated with the study or the Buck Institute noted that while studying animals doesn't necessarily translate into an effective treatment for humans, the Buck research is promising because the mice were given a human strain of Alzheimer's.

Since the mid-1980s, scientists have known that Alzheimer's is associated with the buildup of a sticky plaque around neurons in the brain, and for years research has been focused on how to stop the plaque from being created. But the Buck Institute scientists allowed the plaque to build up and still found a way to stop it from affecting the mice memories.

The key was focusing on a protein, called the amyloid precursor protein. The protein is made up of 695 amino acids, and when the protein is cut into pieces at the 595th and 635th amino acids, the plaque is created.

The Buck scientists turned their focus away from the 595th and 635th amino acids, and instead focused on the tail end of the protein -- the last 31 amino acids, known as C31 -- which also is cut from the protein. The scientists replaced a single amino acid in that strain, which stopped the C31 section from being cut off.

Buck scientists can't explain exactly why it works, but preventing the C31 section from being severed seems to result in Alzheimer's symptoms never showing up. Even at the "old age" of 18 months, mice that received the treatment were symptom-free. Their mouse counterparts that did not get the amino acid replacement showed symptoms of Alzheimer's by the time they were 3 months old.

"Our mice all had the same Alzheimer's disease, but we simply changed one amino acid out of 695. It's like if you had two houses that are identical and one brick in one house is different," Bredesen said. "It tells us that that particular pathway is a very important one and a good point to target new drugs."