Unraveling the mysteries of Alzheimer’s disease

Four-Parts | PART 2 | PART 3 | PART 4

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s a distinguished professor in the USF Health College of Public Health, Karen Liller’s days are filled with research, teaching and administrative responsibilities. But on the first Thursday of each month, she makes it a priority to participate in a virtual caregivers support group offered by the USF Health Byrd Alzheimer’s Center and Research Institute.

Her reasons are personal, not professional: Liller, MA ’82, EdS ’86 and PhD ’88, is one of the caregivers for a family member with Alzheimer’s disease. Through the support group, she learns about helpful resources and techniques that fellow caregivers have discovered. She extends, and receives, empathy as group members compare notes on their frustrations and those of their loved ones, who suffer both memory loss and the progressive loss of cognitive abilities. Perhaps most importantly, the sessions remind the group members that they are not alone. For Liller, the discussions are cathartic.

That’s important, because as Liller says, “Alzheimer’s is the most demonic disease I can think of.”

According to the Alzheimer’s Association, nearly 7 million Americans are living with the incurable disease – a number that could double by 2060 as the nation’s population ages.

The lifetime risk for Alzheimer’s at age 45 is one in five for women and one in 10 for men. One in three older adults dies with Alzheimer’s or another dementia. Established in 2002, the Byrd Institute is on the front lines of assessments and medical care, clinical trials of new medications and research to understand the changes in the brain that cause Alzheimer’s and other types of dementia, and to develop approaches to prevent and treat Alzheimer’s disease and memory loss.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

There’s not a singular cause of Alzheimer’s, according to Dr. Amanda Smith, director of clinical research for the institute.

“There are a number of risk factors, with age being the biggest,” she says. “There are some people who have a genetic propensity toward it, either because of specific mutations that cause early onset Alzheimer’s or because they carry a gene that infers risk. People who have had head injuries at any point in their life are at higher risk. People with lower levels of education and people who have cardiovascular risk factors have a higher risk.”

Alzheimer’s results from a buildup of amyloid protein, which causes plaque, and tau protein, which causes tangles, in the brain. “As to why it happens to some people and not others, why some people get it at age 55 and some people at 90, that’s all still blurry,” Smith says.

A major focus at the institute is on clinical trials of new medications, such as lecanemab, which was approved by the U.S. Food and Drug Administration last year. While the drug has been shown to slow the progression of Alzheimer’s, it can only be prescribed to patients showing mild cognitive impairment or mild dementia. Risks include brain swelling and bleeding, so patients on certain blood thinners cannot take it.

“There is sometimes an expectation that these medications will make people better and it’s important to temper those expectations,” Smith says. “Although these drugs are removing amyloid, they’re not stopping it completely or reversing it. You are slowing the progression. It’s important that we are very realistic about this.”

From a prevention standpoint, Smith emphasizes the impact lifestyle changes can have on reducing risk factors. “There is a huge body of data showing that physical activity, a healthy diet, all of these lifestyle interventions that people can do have a dramatic effect on risk,” she says.

“Those interventions can actually slow cognitive decline.”

A 2023 study conducted by the University of Sao Paulo Medical School in Brazil found that consuming more than 20% of daily calories from ultraprocessed foods — filled with additives such as fats, sugars, artificial flavors and stabilizers — affected cognition. The study found that, in general, people who consume the most ultraprocessed foods have a 28% faster decline in cognitive scores.

A separate study found that eating about two servings per week of processed red meat — such as bacon, bologna and hot dogs — raises the risk of dementia by 14% compared to those who eat less than three servings a month. The study included more than 130,000 people who were followed for up to 43 years.

“The brain is not as privileged an organ as we thought a few years ago,” says Gopal Thinakaran, CEO of the Byrd Institute, Eric Pfeiffer Endowed Chair in Alzheimer’s Research and professor of molecular medicine in the USF Health Morsani College of Medicine.

“What you eat gets to your brain, whether you exercise or not makes a huge difference through blood circulation and the metabolites that are carried to the brain.”

Sleep also plays a role.

“There was a landmark study that measured how much amyloid is coming through during the day and during the night,” Thinakaran says. “What they found was remarkable: That when we sleep our brain is actually actively clearing out amyloid and when we are awake, our brain is active and the neural activity increases amyloid plaque production.” Much of Thinakaran’s research over the past decade has focused on a gene known as BIN1.

“People who have certain variations in this gene are at higher risk for Alzheimer’s disease,” he says. “If you are carrying these variations, if you are not taking care of what you eat or how much you exercise, that adds up to pushing you toward being more susceptible to Alzheimer’s disease.” 

About 50 genes exhibit the variations. “One person may have variants in genes 1, 5 and 10, and another person may have variants in genes 7, 12 and 20,” he says.

“How that elevates one’s lifetime risk really depends on the lifestyle choices we make.”

Like Thinakaran, many researchers are working to understand the genes’ biology so they they can identify the most effective preventative measures affected individuals can take.

They’re also exploring other biological factors, including the connection between vascular health and Alzheimer’s.

“I’ve been doing this for 22 years and the progress we’ve made in the last few years has been incredible,” Smith says. “For the longest time, it was the same thing — no new drugs, lots of failures in the clinical trial realm. Now, we have blood tests, we have imaging tests, we have more ways to accurately diagnose the disease and then provide effective treatment.”

Though no cure exists, “We’re closer than we were when I started this work,” she says, “and that’s what brings me here every day.” 

Stories by Tom Woolf // University Communications and Marketing