Jim Fisher, a Vietnam veteran, was trying to buy his youngest son his first car. But when he was asked for his Social Security number, he hesitated and said he couldn't remember it. He couldn't remember his birth date either.
That was nearly two decades ago. Because of his age – Jim was 49 at the time – dementia wasn't even considered as the cause. Doctors diagnosed him with depression, believing it stemmed from his combat history. But treatment didn't work, and Jim continued to decline.
"Jim loved to read "Star Trek" books, but he kept buying duplicates," his wife recalled. "One day, I found him writing a grocery list, and I noticed the letters were there to make up words, but they were all in the wrong order."
The symptoms continued, and eventually doctors diagnosed Jim with early-onset Alzheimer's disease.
While Jim's story is unusual because of his age, the cognitive decline experienced by those with dementia is all too well-known. And unlike heart disease or cancer, there are no treatments available for the prevention or cure of Alzheimer's, which is an 100 percent progressive and fatal disease.
But that doesn't mean there is no hope.
Alzheimer's researchers and other experts will discuss a slew of potential future therapies this week at the Alzheimer's Association International Conference in Vancouve. The discussions come on the coattails of the U.S. Food and Drug Administration approval of Eli Lily's Amyvid -- a drug designed to help doctors zero in on the toxic culprit believed to cause brain cell death in Alzheimer's disease, a protein called beta-amyloid.
Many of these treatments are in a class of drugs that act in a similar fashion to vaccines, using the body's own immune system to attack beta-amyloid. Two of these drugs -- Eli Lily's solenezumab and Pfizer's bapineuzamab -- are already in Phase III clinical trials, the last stage of testing before they could potentially be marketed. Roche's Genentech has also recently been investing in a new drug class that will target another Alzheimer's perpetrator known as tau protein -- a substance released from dead neurons thought to also contribute to the progression of the disease.
"There is a huge revolution going on in medicine using the immune system to target specific abnormalities in the disease pathway of Alzheimer's," said Dr. Michael Rafii, assistant professor of neuroscience at UC San Diego. Rafii is associate medical director of the Alzheimer's disease cooperative study, a group that has been testing new Alzheimer's therapies for the last 20 years. "Immunotherapy has the potential to prevent Alzheimer's disease."
Alzheimer's disease is the most common form of dementia, affecting more than 5 million Americans, and it is the sixth leading cause of death. It is caused by an accumulation beta-amyloid, a byproduct of normal brain function.
The human brain is made up of more than 100 billion neurons, and by working together, these neurons are able to create and store a lifetime of hopes, dreams, and memories. Faster and more capable than any computer ever made, the brain has the ability to react to its surroundings in less than two tenths of a second and scholars have estimated, store more than three million hours of video data.
Normally, our brains are able to get rid of the toxic substance, but in the Alzheimer's brain, the protein accumulates like yellow plaque on un-brushed teeth, eventually leading to the death of brain cells.