Gary was 25 when he found out his father had Alzheimer's, and he lived with the possibility that he might develop the disease until he was 57. That is when he learned he did not inherit the gene.

His family already saw the grim results of the disease. Gary's grandfather, at age 53, veered into the path of a freight train in 1936. The accident killed his grandmother; his grandfather survived with a few stitches and lived another 10 years.

"My family attributed his disease and forgetfulness to his grief over this accident," Gary said. It was only later, when the next generation began to suffer the same symptoms, that one of his aunts began to suspect something was terribly wrong.

Gary's family and 11 other North American families have mutations in the presenilin 2 gene. They are descendants of Germans who settled in two villages in the Volga region of Russia in the 1760s, and later settled in the United States in the late 19th and early 20th centuries.

Their disease is autosomal dominant, meaning children only need to get one abnormal gene from either parent to inherit the disease, and each child has a 50/50 chance of getting it.

This form of Alzheimer's comprises about 1% of the cases of Alzheimer's worldwide.

"If you have that mutation, so far as we know, you will in fact get that disease," Gary said.

And because of that guarantee, Gary's family and others may soon lead the way to a cure for the disease.

DIAN TRIAL

A clinical trial known as the Dominantly Inherited Alzheimer's Network, or DIAN, is studying families with inherited forms of Alzheimer's to learn more about how the disease progresses.

Funded by a grant from the National Institute on Aging in 2008, DIAN has the largest and most extensive worldwide research network investigating dominantly inherited Alzheimer's, with sites in the United States, Britain and Australia.

Initial results from the study presented at the Alzheimer's Association meeting suggest inherited forms of the disease can be detected as many as 20 years before problems with memory and thinking develop.

They found that, as with people with more common Alzheimer's, people who develop early onset disease experience a drop in amyloid in their spinal fluid and an increase in tau some 20 years before their symptoms appear.

The findings suggest that there is a common pathway between inherited Alzheimer's and late-onset Alzheimer's, said Dr. Randall Bateman of Washington University School of Medicine in St. Louis, who is an associate director of the study.

"That is the pathway we want to treat. If we can interfere with that, we can hopefully prevent Alzheimer's disease," he said.

Drug companies are being selected to test their experimental medicines on these study volunteers because if they have the gene, they are certain to get Alzheimer's.

"It's a huge opportunity," said Dr. Rachel Schindler, an Alzheimer's disease expert at Pfizer Inc, which is developing the drug bapineuzumab with Johnson & Johnson , which is now in late-stage clinical trials.

"It's a window into how early we really can detect the changes related to Alzheimer's disease. Without that window, you'd have to study hundreds of people over a long period of time because only a few of them would end up developing the disease," Schindler said.

If scientists can understand the disease, they can apply much of what they learn to late-onset Alzheimer's, she said.

People in the study are eager to participate in the drug trials, Bateman said. "They are desperate to have treatments for their families."

Marty Reiswig, a 32-year-old minister living near Denver, found out about the study from his brother Matt. Matt told Marty that he had to read a book about the family's disease by Gary Reiswig -- their father's cousin.

After reading the book, "The Thousand Mile Stare: One Family's Journey through the Struggle and Science of Alzheimer's," the brothers agreed that their family would make perfect "lab rats," Marty said.

That is because people in his family, unlike most people who get Alzheimer's, know it's coming, he said.

Marty undergoes annual lumbar punctures to have his spinal fluid checked for levels of amyloid and tau -- the proteins that help predict Alzheimer's progression -- and because he has no symptoms, he has a battery of memory tests every three years.

"Because I am a child of an affected early onset Alzheimer's person, they want to study my mental health progress," Marty said.

Marty's and Matt's father Lawrence is also part of the study.

Marty says he relishes his visits with Dr. Bateman, and loves to pepper him with questions about the study.

In one recent visit, he got some good news.

"I was lying in bed with lumbar puncture in my back, talking to Dr. Bateman," Marty recalled. "He said, 'I think some time in the next 12 months, there is a very good possibility we might be doing clinical trials with you to find drugs to prevent the onset of Alzheimer's."'

Marty said he lay in the hospital bed and wept.

"My dad was across from me in the hospital room and we had to control ourselves. That this terrible thing could possibly sort of vanish... that was just a huge relief for us."

"That was thrilling," said Lawrence, who is 58 and just starting to show signs of Alzheimer's.

"He is still very functioning, but worsening," Marty says of his father, who lives in Greeley, Colorado, with his mother Bonnie. "It has most affected his speech."

Lawrence says it takes about five minutes to get himself a bowl of cold cereal and a spoon in the mornings, largely because he gets distracted so often.

"He has a fantastic attitude. He laughs at himself and allows others to laugh about his mistakes," Marty said. "Here he is, faced with this cruel, slow ending to his life, and the embarrassment factor is huge."

When people are in their 90s and make social gaffes, people tend to excuse them, Marty said. "'When you make those same social mistakes at age 58, the people who know what is going on give you grace, but everyone else wonders what is wrong with you."'