New Theory on the Cause of Alzheimer’s Progression

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Researchers say Alzheimer’s disease may start in several areas of the brain, rather than spreading from a single region. Tom Werner/Getty Images
  • Scientists say they believe Alzheimer’s disease may spread differently in the brain than previously thought.
  • They say Alzheimer’s starts in different regions of the brain, rather than spreading from a single area.
  • Experts say the research could lead to better diagnosis as well as new treatments for the disease.

Scientists say they may have discovered that Alzheimer’s disease progresses differently in the brain than previous research suggests.

Researchers from the University of Cambridge in England and Harvard Medical School in Massachusetts report that they believe Alzheimer’s doesn’t begin in a single area of the brain before spreading to other regions.

They say instead that by the time Alzheimer’s starts to grow, it is already present in multiple regions of the brain.

“The thinking had been that Alzheimer’s develops in a way that’s similar to many cancers: The aggregates form in one region and then spread through the brain,” Georg Meisl, PhD, first author of the paper and a researcher from Cambridge’s Yusuf Hamied Department of Chemistry, said in a press release.

“But instead, we found that when Alzheimer’s starts, there are already aggregates in multiple regions of the brain and so trying to stop the spread between regions will do little to slow the disease,” he explained.

The researchers conducted their study using PET scans of those living with Alzheimer’s disease, together with postmortem samples of the brain from people who died with the disease.

They tracked the spread of tau, a type of protein that contributes to Alzheimer’s.

In Alzheimer’s disease, tau and another protein called amyloid-beta form tangles and plaques known as aggregates that cause the brain to shrink.

“Amyloid deposits in the brain first, then tau aggregates begin to occur. Neuronal damage later develops, then clinical symptoms of memory loss, and finally, loss of functional independence known as dementia occurs,” Dr. Sharon Sha, a clinical associate professor of neurology and neurological sciences at Stanford University in California, told Healthline.

“The two proteins are thought to predate clinical symptoms by decades. Tau, specifically, because it deposits later in the disease process, may more closely align with clinical symptoms,” she explained.

The researchers found that the progression of Alzheimer’s disease is based on the replication of these aggregates in single regions of the brain, not the spread of the aggregates from one area to another.

They say their study could help improve treatments for Alzheimer’s disease by targeting and stopping the replication of aggregates in the brain.

“The key discovery is that stopping the replication of aggregates rather than their propagation is going to be more effective at the stages of the disease that we studied,” Tuomas Knowles, PhD, co-senior author of the study and a researcher from the Department of Chemistry at Cambridge, said in a press release.

Rebecca Edelmayer, PhD, senior director of scientific engagement at the Alzheimer’s Association, said the findings could have important implications for developing better drugs for the treatment of Alzheimer’s disease.

“This research is particularly informative for tau-targeting drug development. For example, a drug that blocks the buildup of tau in multiple regions of the brain may be more effective than a drug trying to prevent the spread of tau from cell to cell. Bottom line, the hallmarks that define Alzheimer’s disease are complicated and diffuse, and we need drugs that can appropriately target the biology,” she told Healthline.

Up until now, much of the research on Alzheimer’s disease has been in animal models. But this method has flaws.

“Animal models are a great way to learn about disease in living subjects. However, the physiology and development of disease in humans are not directly matched with animal models,” Sha said.

“We often do not see Alzheimer’s disease develop naturally in animals and thus, create ‘synthetic’ Alzheimer’s disease in animals and then try to study or cure them,” she added. “As such, there is an inherent flaw in directly ascribing any disease modeling or treatment based solely on animal models of Alzheimer’s disease.”

For the first time, the Cambridge and Harvard researchers used human data to track the progression of the disease.

Sha is hopeful the study moves researchers one step closer to finding better treatments for Alzheimer’s that stabilize the condition or even cure it entirely.

“I honestly believe that we will have treatments that will allow patients to live healthily and be stable with the disease. Reversing the disease process may be very difficult and reversing the damage done to the brain may be even harder to attain. However, I believe that we are closer, possibly within the next decade, to find ways to live meaningful and healthy lives,” she said.

“As we have seen for cancer and AIDS, treatments can become tailored to the individual based upon the type of syndrome and disease-specific markers,” she noted. “I hope Alzheimer’s disease treatments can be similarly tailored and stabilize, reverse, or even cure disease.”

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