A new, breakthrough study could illuminate promising pathways for treating Alzheimer's disease.

By comparing the genetic profiles of nearly 75,000 people (some with Alzheimer's and some without), an international group of researchers uncovered 11 new genes linked to the disease. When combined with the results of earlier investigations, these recent findings bring the total number of known Alzheimer's-related genes to 21.

Julie Williams, Ph.D., co-author of the study and head of neurodegeneration at Cardiff University in Wales, U.K., says the discovery is promising because it gives researchers further insight into what causes Alzheimer's, though there's still some significant work left to be done. "A large portion of the disease remains unexplained," she says. "Further research is still needed to locate the other genes before we can get a complete picture." Williams and her team are part of the International Genomics of Alzheimer's Project (IGAP), a multi-country collaboration aimed at unlocking the genetic code of Alzheimer's.

Researchers agree that one of the most intriguing findings was the obvious role played by the immune system in contributing to Alzheimer's. Several of the genes linked to the disease were also essential regulators of the immune response. Inflammation triggered by the immune system has been thought to contribute to brain cell death and cognitive decline in people with dementia. These new results lend additional weight to this theory.

Despite being the sixth leading cause of death in the United States, little is known about the biological mechanisms that underlie Alzheimer's disease—why it strikes, who it strikes and how it affects the brain. There are consequently many Alzheimer's myths that people believe.

Families of those with Alzheimer's are intimately familiar with the outward effects—behavioral outbursts, hallucinations, memory loss. But the disease process itself largely remains a mystery, forestalling efforts to develop effective therapies to combat it.

Scientists currently believe that the disease is caused by a confluence of events, including a build-up of neuron-clogging beta-amyloid protein plaques, the creation of communication-clogging tau tangles and the onset of cell-killing inflammation.

Williams told U.K. newspaper, the Daily Mail, that pinpointing the genes that increase a person's chances for developing Alzheimer's could eventually help doctors identify at-risk individuals early, before the disease progresses too far, and prescribe targeted therapies to treat it.

Such therapies are years away from becoming a reality and won't be much help to those who currently have the disease. This is one of the hard truths that caregivers should know about Alzheimer's research.

To learn more about the real-life impact of Alzheimer's on the lives of those with the disease and their families, visit Fade to Blank: Life Inside Alzheimer's.