Significant breakthroughs may come in next decade, experts say.

A new element has emerged in the seemingly never-ending battle against Alzheimer’s disease: hope.

While no one presented a breakthrough along the lines of a Salk vaccine, many of the professionals who attended the ninth international conference on Alzheimer’s Disease in Philadelphia this past summer predicted a viable treatment within the next 10 years.

“Our goal of delaying the disabling symptoms and eventually preventing Alzheimer’s is a feasible objective that we now believe the research community can achieve in the next decade,” Sheldon Goldberg, the association’s CEO, said.

And Shane S. Bush, a psychologist who is president of the neuropsychology division of the New York State Psychological Association, said that finding a treatment for the debilitating memory-affecting disease probably would not come all at once. “Many of the researchers and health-care providers I spoke to were excited to see our understanding of Alzheimer’s disease continue to grow piece by piece,” he said.

An estimated 4.5 million Americans now have Alzheimer’s disease, with millions more in the Baby Boomer generation about to enter the age of greatest risk for the disease - after 65. Without a cure, the Alzheimer’s Association estimates, between 11 million and 16 million Americans will have Alzheimer’s disease by 2050.

Dr. Sam Gandy, vice chair of the National Medical and Scientific Advisory Council of the Alzheimer’s Association and director of the Farber Institute for Neurology at Thomas Jefferson University in Philadelphia, agrees the next five to 10 years are likely to bring significant advances in both diagnosis and treatment of this presently irreversible condition.

Gandy is among the researchers who see the key to Alzheimer’s may lie with the diagnosis and treatment of plaques and other abnormal protein aggregates called “tangles” in the brain, which many scientists think might be the hallmarks of Alzheimer’s. The main component of plaques, a toxic protein fragment called beta-amyloid, is a primary suspect in the death of brain cells, which causes the mental deterioration that marks the condition.

He cites a breakthrough by Dr. William E. Klunk and his colleagues at the University of Pittsburgh. They recently developed a compound known as Pittsburgh Compound-B (PIB) that sticks to amyloid plaques and makes them visible on positron emission tomography (PET) scans for the first time. According to Gandy, the ability to finally view, monitor and measure amyloid probably heralds the beginning of a new chapter in Alzheimer’s research.

“Combined with advances in medications to rid the brain of amyloid plaques, this could very well result in a major breakthrough in our understanding of and successful treatment of Alzheimer’s,” Gandy said. “It will not only answer questions about how amyloid damages brain cells, but it will help us monitor whether and how well the new medications work.”

According to Gandy, as PET technology becomes more widespread, it will be increasingly possible to test the hypothesis that amyloid is the primary culprit in Alzheimer’s.

“Our inability to visualize or measure amyloid in the brain was a huge bottleneck for research,” Gandy explained. “Now that there are both medications that can rid the brain of amyloid and a method of visually monitoring the amount of amyloid present and the effect of the medication on it, we’re about to move past that bottleneck once and for all. We should know very soon whether amyloid is the right target or whether our focus on it has been a huge mistake.”

Gandy admitted that the amyloid hypothesis isn’t the only one being rigorously pursued by the medical community.

“There are other models - potential explanations - for what causes Alzheimer’s,” he said. “Some researchers are looking closely at abnormal oxidation and the role it may play in the aging of brain cells, for example.”

“There is some evidence that the accumulated damage from oxidation could result in the cognitive impairments characteristic of this disease, just as oxidation affects the condition of other cells in the body.”

Gandy also pointed out that evidence is building about what he termed “softer” factors related to Alzheimer’s risk and its reduction.

“Lifestyle factors,” he said. “It’s become clear that lifestyle factors that are bad for the heart are also bad for the brain. Cholesterol, obesity, diabetes - these take their toll on the brain. Living a healthy, mentally and physically active lifestyle turns out to be a fairly good way to protect brain cells and, potentially, prevent Alzheimer’s.”