A new theory about the causes of the progression of Alzheimer’s disease

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• Scientists say they believe that Alzheimer’s disease can spread to the brain in a different way than previously thought.
• They say that Alzheimer’s disease does not spread from a single area, but begins in different areas of the brain.
• Experts say the study may lead to better diagnosis and new treatments for the disease.

Scientists say they may have discovered that Alzheimer’s disease progresses in the brain in a different way than previous studies suggest.

Researchers at the University of Cambridge in the United Kingdom and Harvard Medical School in Massachusetts report that they believe that Alzheimer’s disease does not begin in a single area of ​​the brain before it spreads to other areas.

Instead, they say that by the time Alzheimer’s disease begins to grow, it is already present in multiple regions of the brain.

“The idea was that Alzheimer’s disease develops in a similar way to many cancers. Aggregates form in one area and then spread throughout the brain.” Georg Meissle, PhD, the first author of the dissertation, and a researcher at the Department of Chemistry, Cambridge University, Cambridge, said in a press release.

“But instead, when Alzheimer’s disease begins, there is already aggregate in multiple regions of the brain, so trying to stop the spread between regions rarely delays the disease,” he explains. bottom.

Researchers are their study Use PET scans of people with Alzheimer’s disease, along with postmortem samples of the brains of people who died of Alzheimer’s disease.

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

of Alzheimer’s diseaseAnother protein, called tau and amyloid beta, forms tangles and plaques known as aggregates that contract the brain.

“First amyloid deposits in the brain, then tau aggregates begin to develop. Later nerve damage occurs, then clinical symptoms of memory loss occur, and finally, functional independence known as dementia. Sexual loss occurs. ” Dr. SharonshaA clinical associate professor of neurology and neuroscience at Stanford University, California, told Healthline.

“The two proteins are thought to exist decades before clinical symptoms. Tau may be more closely aligned with clinical symptoms, especially because it deposits later in the disease process.” She explained.

Researchers have found that the progression of Alzheimer’s disease is based on the replication of these aggregates in a single area of ​​the brain, rather than the spread of the aggregates from one area to another.

They state that their work may help improve the treatment of Alzheimer’s disease by targeting and stopping the replication of aggregate in the brain.

“The important finding is that stopping replication rather than transmitting aggregate is more effective at the stage of the disease we studied.” Zomas KnowlesThe co-chief author of the study and a PhD researcher in the Department of Chemistry in Cambridge said in a press release.

Rebecca EdelmeierThe doctor’s degree, senior director of scientific involvement in the Alzheimer’s Disease Association, said the findings could have important implications for the development of better drugs for the treatment of Alzheimer’s disease.

“This study is particularly useful for drug development targeting tau. For example, drugs that block the accumulation of tau in multiple areas of the brain are better than drugs that try to prevent the spread of tau from cell to cell. It may be effective. In conclusion, the characteristics that define Alzheimer’s disease are complex and diffuse, and we need drugs that can properly target biology, “she told Healthline.

To date, much of the research on Alzheimer’s disease has been done in animal models. However, this method has its drawbacks.

“Animal models are a great way to learn about the diseases of living subjects, but the physiology and development of human diseases are not in direct agreement with animal models,” Sha said.

“We often don’t see Alzheimer’s disease occurring spontaneously in animals, so we cause” synthetic “Alzheimer’s disease in animals and then try to study or treat them,” she added. “Therefore, there are inherent flaws in directly modeling or treating the disease based solely on the animal model of Alzheimer’s disease.”

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

Sha hopes that this study will bring researchers one step closer to finding better treatments to stabilize and even completely cure Alzheimer’s disease.

“I honestly believe that there are treatments that can help patients live healthy and stabilize their illness. It can be very difficult to reverse the process of illness, based on the damage done to the brain. It can be even more difficult to get back to, but we believe we’re probably approaching finding a way to live a meaningful and healthy life within the next decade, “she said. rice field.

“As we’ve seen about cancer and AIDS, treatments can be tailored to the individual based on the type of syndrome and disease-specific markers,” she said. “I hope that the treatment for Alzheimer’s disease can be adjusted in the same way to stabilize, reverse and even cure the disease.”

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