TORONTO — There is hopeful news from the efforts to devise a vaccine to prevent and possibly reverse early cases of Alzheimer's disease.

Two studies, published Sunday in the journal Nature Medicine, suggest the vaccine is still a viable option, despite the fact that a clinical trial of a candidate vaccine was abruptly halted early this year when a small portion of the subjects developed inflammation on the brain.

The first paper, from a group of scientists in Zurich, Switzerland, reported that blood and spinal cord fluid samples taken from some of the study participants show their immune system had produced antibodies to fight the amyloid plaques which have been called "the primary villain" of the disease.

In other words, in a portion of the patients, the vaccine did what it was hoped it would do -- it prompted the subject's immune system to see the peptide which is the building block of the plaque as a threat which needed to be attacked.

"Clearly, further research is required to improve the safety of this novel therapeutic strategy," Dr. Roger Nitsch, director of psychiatric research at the University of Zurich and one of the Zurich authors, said in a statement.

"Our patients are now carefully followed up to determine whether the vaccination is effective in preventing cognitive decline and progression in dementia."

The second paper, written by the research team from the University of Toronto which came up with the initial vaccine, suggests a way to refine it so as to avoid the inflammation problem which halted the clinical trial.

Taken together, the articles may restore faith in the potential of a vaccine as a way to combat the heartbreaking disease, which kills nerve cells in the brain leading to memory loss, cognitive decline and eventually death.

"It shows the viability of the antibody approach," said Einar Sigurdsson, a professor of psychiatry and pathology at New York University who is working on an alternative vaccine at that institution, said of the Toronto paper.

"And it shows that if you focus on certain epitopes" -- a piece of a peptide, not the entire peptide -- "you might be able to prevent the inflammation. But it doesn't really prove it at this point."

Nor does the Zurich paper address the crucial question arising from the halted clinical trial, Sigurdsson said.

"It doesn't answer the main question that is in everybody's mind: Why did they develop inflammation?"

The clinical trials, undertaken by Dublin-based Elan Corporation and Wyeth-Ayerst Laboratories, tested a vaccine first proposed by a team of researches from the Centre for Research in Neurodegenerative Diseases at the University of Toronto.

The team, led by Peter St. George-Hyslop, published a paper in Nature in December 2000 showing their vaccine had worked in mice bred to have the mouse model of Alzheimer's disease.

The vaccine had been shown to be safe in humans in a small Phase 1 trial. It was only when a larger Phase 2 trial was undertaken, with several hundred patients in the United States and Europe, that the problem of inflammation in the brain was noted in a number of participants.

When the Toronto team learned of the problem, they went back to work to see if they could find a way to modify the vaccine in order to side-step the problem.

The initial vaccine used the entire peptide, which is a sequence of 42 amino acids. The Toronto team now believes that if only a portion of that sequence was used, the vaccine would induce the desired immune response without triggering the unwanted side-effect, said lead author JoAnne McLaurin, a professor of clinical biochemistry at the university.

"Basically we've identified an area where we can refine the vaccine now, is really what we've done," she said.

Pinpointing the necessary portion of the peptide has another, longer term benefit. The team will try to figure out how that sequence of amino acids interacts with the immune system with the aim of developing a drug that mimics the effect, "so we can circumvent immunotherapy completely," McLaurin said.

That has appeal because immunotherapy only works well if a vaccine can provoke a strong reaction in the person who receives it. And it's well known that the older one gets, the less robust one's immune system is.

"A pill is so much easier to do," McLaurin said. "There are a lot of extra steps in immunotherapy which you wouldn't have to worry about with a drug.

"It's the first time that we've known an area to target specifically. That's why this is quite novel," she said, noting that while such a drug should be "quite easy" to develop, it would be at least five to 10 years before anything would hit the market -- if their efforts come to fruition.