New research identifies the cause of Alzheimer’s disease progression

  • New research suggests that Alzheimer’s disease is developing differently than previously thought.
  • The findings showed that tau protein clusters replicate in several regions of the brain at one time rather than starting from one region and then spreading to another.
  • The results could pave the way for the development of treatments that slow the progression of the disease.

Revolutionary research sheds new light on the progression of Alzheimer’s disease in the brain, influencing future treatments and prevention strategies.

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

By 2060, that number is expected to grow to 14 million.

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

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

According to researchers, data from humans for the first time show that Alzheimer’s disease develops differently than previously thought.

A study by the University of Cambridge in October 2021 found that instead of protein aggregates (protein clumps) appearing in one area before spreading to another, they replicate in several areas of the brain at once.

These toxic protein aggregates, known as tau, replicate and destroy brain cells, causing symptoms such as memory loss and confusion that eventually become more severe and fatal as Alzheimer’s disease progresses.

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

“It was hypothesized that the spreading process would be a crucial step in controlling the rate of protein aggregation and deposition in the disease,” he said.

The researchers concluded that early interventions to limit local replication of protein aggregates may slow disease progression.

“The results suggest that we should look for ways to slow the replication of tau rather than focus on proliferation — this is a new concept,” David A. Merrill, MD, PhD, adult and elderly psychiatrist and director of the disease. The Pacific Brain Health Center at the Pacific Neuroscience Institute told Psych Central.

A new study points scientists and pharmacologists in a different direction.

“There may be ways to intervene and stop a mechanism that facilitates tau replication and aggregation, or to find a blocking mechanism that does not allow tau to aggregate and develop drugs based on such a mechanism,” said Michal Schnaider Beeri, PhD, a geriatric psychologist. and Professor of Psychiatry at Icahn School of Medicine in Mount Sinai.

According to Merrill, “If you could slow down the replication of tau by five years, you would reduce the incidence of more serious Alzheimer’s disease.”

Modern treatment for Alzheimer’s includes cognition-enhancing medications and strategies to control symptoms.

Recent therapeutic developments have focused on targeting beta-amyloid (plaque), a feature of Alzheimer’s disease. However, a a key concern The targeting of these plaques is that not all dementia patients have them.

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

“The FDA’s recently approved medication eliminates one of the characteristic pathologies of Alzheimer’s disease (amyloid plaques), but shows little evidence of improved cognition,” he said. “The results of this study suggest a different direction for new therapies.”

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

While the findings are relevant to the development of new therapies, they may not be important in the development of preventive approaches, according to Knowles.

“We cannot rule out the possibility that the spread may be relevant in the early stages of the disease, and we are actively working to investigate this issue,” Knowles said.

The results also promise to understand other diseases of protein aggregation, such as Parkinson’s disease.

“Most existing therapeutic candidates for tau aggregation, especially those based on antibodies, are targeting a proliferation phase that we believe [new] the analysis is unlikely to be an effective target, ”Knowles said.

While research may lead to new treatments that help preserve memory and prolong life, it is unclear whether Alzheimer’s can ever be completely eradicated.

Meanwhile, doctors say certain lifestyles, such as regular aerobic exercise and a Mediterranean diet, can help prevent or slow the progression of the disease.

Medical strategies such as controlling blood pressure and blood sugar levels can also help.

“It will be interesting to see if any of these approaches really target tau replication,” Merrill said. “It’s certainly an exciting time, and these findings will help us move forward to a better understanding of what’s important in the disease process.”


Leave a Comment