With no drugs or treatments stopping, or even slowing the effects of Alzheimer's, some scientists are stepping back to gain a new perspective.

An expert on brain disease, Dr. Dale Bredesen told the San Francisco Chronicle about a well-known analogy for Alzheimer's and how it could help someone find a solution. A house with holes in the roof is going to get wet and if you only fix one hole, the floor is not going to dry. The human brain is the same way.

To help cure Alzheimer's - or prevent it in the first place - would require doctors and experts to patch all the holes in the roof and not just one.

"If you look at the basic mechanisms that lead to abnormalities and disease, there might be 36 different mechanisms," said Bredesen, a scientist with the Buck Institute for Research on Aging in Novato. "Maybe we need to do more than patch one hole at a time."

The amyloid beta has been considered to be a hole in the roof for decades and has been a target of research as a result. Amyloid is a protein in the brain that is known to tip doctors off when it begins to form in distinctive clusters.

The post-WWII Baby Boomers are hitting the later stages of their lives more and more, applying pressure to experts to come up with a cure or preventative solution. Doctors believe the amount of care required for Alzheimer's patients will put an emotional burden on their loved ones and financial stress on healthcare insurances nationwide.

"All of us who take care of patients wish that things could move at a faster pace," said Dr. Gil Rabinovici, a neurologist in UCSF's Memory and Aging Center. "In Alzheimer's we're really pretty far behind the curve. This is an impending public health crisis, and it would be very rational for us to invest in a lot of different ideas about how to treat the disease."

While genetics plays into Alzheimer's as much as degeneration brought on by old age does, researchers are still looking to find new ways to reverse the disease's slowly progressing effects. Experts at Stanford are studying the formation and destruction of synapses.

Synapses form to help humans learn new skills and retain memories, but they must also be destroyed to maintain efficiency and proper working order. In Alzheimer's patients, those synapses stop working properly and their destruction processes become overactive.

"The current idea is the sickness starts earlier" than believed before, said Carla Shatz, a Stanford neurobiologist. "The real loss is in the loss of synapse connections."