The faces of Alzheimer's Part IV: Face of the researcher and the future
This is the final part of a four-part series examining how Alzheimer’s disease affects the patient, the family and the public. The Pine Journal ran this series each week in November to coincide with National Family Caregiver Month.
Scientists are focused on curing Alzheimer’s disease (AD). Perhaps there’s no cure yet because researchers are dealing with the most intricate and complex organism in the universe: the human brain. Today, Alzheimer’s is at the forefront of biomedical research, with 90 percent of known information about it discovered only in the last 15 years.
How Alzheimer’s affects the brain
Basically, the brain has 100 billion nerve cells. Each nerve cell connects with others to form communication networks. In doing their work, brain cells operate like tiny factories. Scientists believe Alzheimer’s disease prevents parts of a cell’s little factory from running well. But they aren’t sure where the trouble starts.
Two abnormal structures, called plaques and tangles, are prime suspects in damaging and killing nerve cells. Plaques are deposits of a protein fragment called beta-amyloid that build up in the space between nerve cells. Tangles are twisted fibers of another protein called “tau” that build up inside cells. Scientists do not know exactly what role plaques and tangles play in AD. Most experts believe they somehow play a critical role in blocking communication among nerve cells and disrupting processes cells need to survive.
For years scientists have known that a small area deep in the brain, called the hippocampus, loses many of its cells at the beginning of Alzheimer’s disease. As the disease progresses, cells in other areas die in a predictable pattern paralleling the progression of Alzheimer’s symptoms.
One research project underway (Breakthrough, “Decoding the Brain,” National Geographic Channel) involves implanting a deep brain stimulus, whose duty is sending impulses to the hippocampus, in an effort to suppress epileptic seizures. Early results are favorable. Every new piece of information learned about the hippocampus will benefit future Alzheimer’s research.
Certain drugs approved by the FDA treat cognitive symptoms of AD. Effectiveness varies from person to person. While they may temporarily help symptoms, they do not stop brain changes causing Alzheimer’s to become more severe over time. Hope should never be lost for a drug that will slow the disease or stop it from progressing.
Prescription medications used to treat behavioral and psychiatric symptoms, resulting from progressive damage to brain cells, can be effective but are medically challenging. Their use should be closely supervised. Drug research targeting beta-amyloid, the protein fragment that builds up into plaques, suggests they can be cleared from the brain or prevented from forming.
(Source: Alzheimer’s Association)
Another developing area of research involves transplanting brain tissue or growing new brain tissue using stem cells. Stem cell research was initially controversial mainly because stem cells were harvested from aborted human fetuses. However, adult stem cells are proving to be just as effective, thus avoiding the ethical conflict from using fetal tissue.
A Duluth News-Tribune article (9/22/2015) offers hope that research is progressing toward finding a cure. The article, “New Alzheimer’s trial uses epilepsy drug that calms brain activity,” discusses how the drug AGB101, used to treat epilepsy, might be useful in low doses to reduce the brain over-activity causing it to atrophy.
Promising early research by John Hopkins University and startup drug company AgeneBio successfully showed low dose treatment of AGB101 to lab animals, like rats, resulted in calmed over-activity in the brain and improved memory performance in subjects experiencing memory loss and considered pre-dementia.
The National Institute on Aging, a division of the National Institute of Health, has put up $7.5 million to help fund the five-year clinical trial study which could lead to the drug’s approval by the FDA in 2020. The drug will be tested over this five-year period on hundreds of patients around the world.
Although John Hopkins will run the clinical trial program, it does not benefit financially from the partnership with AgeneBio, which will cover the bulk of trial expenses. AgeneBio must make ALL research data public as part of the deal.
Since Alois Alzheimer first described this disease in 1906, average lifespan has increased from 50 years to nearly 80, but life-altering research breakthroughs remain elusive. Now, major results could be on the horizon. If AGB101 or another drug proves successful, it could revolutionize treatments and outcomes for people with Alzheimer’s.
People knew little about Alzheimer’s when Ronald Reagan disclosed he had it in 1991. Today, they are more knowledgeable.
The Act on Alzheimer’s movement, designed to make governments, businesses, police, and the public dementia-friendly, is organizing in communities across Minnesota (Pine Journal, 9/18/14, and Duluth News-Tribune, 11/3/2015).
An example of dementia-friendly was related by Edina’s Victoria Bresson at her father’s funeral Nov. 2. Victoria, a grief counselor, spoke openly and eloquently about her dad’s battle with Alzheimer’s. Married after World War II, he provided well for his future. As Alzheimer’s progressed, he needed reassurance his savings were secure.
The bank statements came monthly, but he quickly forgot he’d received them. Victoria visited her parents often, and at each visit she’d take him to his bank, where employees greeted him with, “Hi Art, we haven’t seen you for awhile.” And each time they’d make copies of his statements for him. They understood Alzheimer’s disease, and were sympathetic to Art like dementia-friendly businesses should be in dementia-friendly towns like Cloquet.
A note from the author
On this Thanksgiving Day, I want to thank everyone who contributed to this series, especially Kristine Dwyer for her advice and support, and Candi, Donna and Ernie from the support group for their openness. I’ve been blessed to find friendship among many Alzheimer’s patients and their families. I also want to thank the Pine Journal’s editor, Jana Peterson, for believing this series will increase the public’s awareness about Alzheimer’s. Although providing only “tip of the iceberg” information, we gave people a place to start their battle should their family face Alzheimer’s.
Finally, God puts us in situations to help another. I’ve wondered for months, “Why was I drawn to learn about Alzheimer’s?” Undeniably, there’s vulnerability in the AD patient which makes me want to help. But one month ago I learned why. My best friend in the world was diagnosed with Alzheimer’s. I understand now what God wanted me for — that I should help my friend and his family. I thought writing this four-part series was hard, but the hard part has just begun.