New theory on the cause of the progression of Alzheimer’s disease

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Researchers say Alzheimer’s disease can start in multiple regions of the brain, rather than spreading from just one region. Tom Werner / Getty Images
  • Scientists say they believe Alzheimer’s disease can spread in the brain differently than previously thought.
  • They say Alzheimer’s disease starts in different regions of the brain, rather than spreading from a single area.
  • Experts say the research could lead to a 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 at the University of Cambridge in England and Harvard Medical School in Massachusetts report that they believe Alzheimer’s disease does not start in one area of ​​the brain before spreading to other areas.

Rather, they say that by the time Alzheimer’s disease begins to develop, it is already present in several areas of the brain.

“The idea was that Alzheimer’s disease develops in a way similar to many cancers: aggregates form in one region and then spread throughout the brain,” said Georg Meisl, PhD, lead author of the Cambridge article and researcher Yusuf Hamied. Chemistry, said in a press release.

“But instead, we found that when Alzheimer’s disease starts, there are already aggregates in several areas of the brain, and so trying to stop the spread between areas won’t do much to slow the spread. disease, ”he explained.

The researchers conducted their study using CT scans of people living with Alzheimer’s disease, as well as post-mortem brain samples from people who died from the disease.

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

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

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

“Both proteins are thought to predate clinical symptoms by decades. Tau, in particular, because it is deposited later in the disease process, may align more closely with clinical symptoms, ”she explained.

Researchers have found that the progression of Alzheimer’s disease is based on the replication of these aggregates in unique regions of the brain, not on 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 finding is that stopping the replication of aggregates rather than spreading them will be more effective at the stages of the disease we have studied”, Tuomas Knowles, PhD, study co-lead author and researcher in the Department of chemistry in 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 the development of better drugs for the treatment of Alzheimer’s disease.

“This research is particularly instructive for the development of drugs targeting tau. For example, a drug that blocks the buildup of tau in multiple areas of the brain may be more effective than a drug that tries to prevent the spread of tau from cell to cell. Ultimately, the defining characteristics of Alzheimer’s disease are complicated and diffuse, and we need drugs that can appropriately target biology, ”she told Healthline.

So far, much of the research on Alzheimer’s disease has been done in animal models. But this method has flaws.

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

“A lot of times we don’t see Alzheimer’s disease developing naturally in animals and thus creating ‘synthetic’ Alzheimer’s disease in animals and then trying to study or cure them,” she added. . “As such, there is an inherent flaw in directly attributing any disease model or treatment based solely on animal models of Alzheimer’s disease.”

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

Sha hopes the study will bring researchers closer to finding better treatments for Alzheimer’s disease that stabilize the disease or even cure it completely.

“I honestly believe that we will have treatments that will allow patients to live healthy lives and be stable with the disease. Reversing the disease process can be very difficult, and reversing the damage to the brain can be even harder to achieve. However, I think we are closer, maybe over the next decade, to finding ways to live healthy and meaningful lives, ”she said.

“As we have seen for cancer and AIDS, treatments can be tailored to the individual depending on the type of syndrome and specific markers of the disease,” she noted. “I hope that the treatments for Alzheimer’s disease can be adapted in the same way and stabilize, reverse or even cure the disease.”


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