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  • A new study suggests Alzheimer’s develops differently than previously thought.
  • Findings showed that tau protein clumps replicate in multiple regions of the brain at once, rather than starting in one area then spreading to another.
  • Results could pave the way for developing treatments to slow disease progression.

A groundbreaking study sheds new light on how Alzheimer’s disease progresses in the brain, with implications for future treatments and prevention strategies.

Alzheimer’s disease is the most common form of dementia. As many as 5.8 million people have the condition in the United States.

By 2060, this number is expected to increase to 14 million.

Currently, Alzheimer’s disease is among the top 10 leading causes of death in the United States.

A report from the Alzheimer’s Association states that women account for nearly two-thirds of Alzheimer’s cases in the United States, and older Black and Hispanic Americans are more likely to have Alzheimer’s and other dementias than their white counterparts.

According to researchers, for the first time human data shows that Alzheimer’s develops differently than previously thought.

The October 2021 study from the University of Cambridge found that instead of appearing in one region before spreading to another, protein aggregates (clumps of protein) replicate in multiple areas of the brain at once.

These toxic protein aggregates, known as tau, replicate and destroy brain cells, causing symptoms like memory loss and confusion, which eventually become more severe and deadly as Alzheimer’s progresses.

“This was a surprise to us and I think many in the community,” study co-author Tuomas Knowles, PhD, professor of physical chemistry and biophysics, told Psych Central.

“It had been assumed that the spreading process would be a crucial step in controlling the rate at which protein aggregation and deposition happens in the disease,” he said.

Researchers concluded that early interventions to limit the local replication of protein aggregates could slow disease progression.

“The results imply that we should look for ways to slow down the replication of tau more so than focusing on spread — this is a new concept,” David A. Merrill, MD, PhD, an adult and geriatric psychiatrist, and director of the Pacific Neuroscience Institute’s Pacific Brain Health Center, told Psych Central.

The new research points scientists and pharmacologists in a different direction.

“There may be ways to intervene and halt the mechanism that facilitates replication and aggregation of tau, or discover the inhibition mechanism that doesn’t allow tau to aggregate and develop medications based on such mechanism,” said Michal Schnaider Beeri, PhD, psychiatry professor and Director of the Joseph Sagol Neuroscience Center at Sheba Medical Center.

According to Merrill, “If you could slow the replication of tau by 5 years, you would decrease the incidence of more severe Alzheimer’s disease.”

Modern Alzheimer’s treatment involves medications that improve cognition and strategies to manage symptoms.

Recent developments in treatments have focused on targeting beta-amyloid (plaques), a defining characteristic of Alzheimer’s. However, a key concern with targeting these plaques is that not all people with dementia have them.

“Today’s treatments have very limited effects,” Beeri said.

“The recently FDA-approved medication clears one of the hallmark pathologies in Alzheimer’s disease (amyloid plaques), but shows little evidence for improving cognition,” he said. “The results of this study propose a different direction of research for new therapies.”

New therapies to treat Alzheimer’s are already emerging — but are not yet targeting tau replication. In fact, Brigham and Women’s Hospital in Boston announced in November that it will soon begin the first human trial on a nasal vaccine to treat the disease. The intranasal vaccine will use Protollin, an immune modulator, to trigger clearance of beta amyloid plaques.

The study focused mainly on the replication of tau. It did not explore other pathologies that cause Alzheimer’s. Additionally, it did not explore the very early stages of the disease.

While the findings are relevant for developing new treatments, they’re not necessarily relevant for developing preventive approaches, according to Knowles.

“We cannot exclude that spreading might be relevant at the very early stages of the disease, and are actively working to investigate this issue,” Knowles said.

The results also hold promise for understanding other protein aggregation diseases, such as Parkinson’s disease.

“Most existing therapeutic candidates against tau aggregation, especially those that are antibody-based, target the spreading step, which according to our [new] analysis, is less likely to be an effective target,” Knowles said.

Though the research could lead to new treatments that help preserve memory and prolong life, it’s unclear whether Alzheimer’s could ever be fully eradicated.

In the meantime, doctors say that certain lifestyle approaches, such as regular aerobic exercise and a Mediterranean diet, can help prevent or slow disease progression.

Medical strategies, like managing blood pressure and blood sugar levels, can also help.

“It’ll be interesting to see if any of these approaches actually target tau replication or not,” Merrill said. “It’s certainly an exciting time, and these findings help move us forward with a better sense of what’s important in the disease process.”