Health

Study identifies therapeutic target for Alzheimer’s disease, revealing strategy for slowing disease progression

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About 11 percent of the U.S. population 65 or above has been diagnosed with Alzheimer’s disease (AD), the most common form of dementia resulting in memory loss and cognitive impairment, according to the Alzheimer’s Association.

And the World Health Organization estimates that the number of people with Alzheimer’s disease will increase by millions each year.

Despite years of research, scientists still do not understand what causes brain damage. And the cure is not known.

But a new study published recently in Environmental communication A team of researchers from Case Western Reserve University School of Medicine has shown that a key protein plays an important role in brain storage. cholesterolcauses the development of Alzheimer’s disease.

Xin Qi Lab, a professor of anthropology and biology at the School of Medicine, coined the patent for the anti-peptide in the first place with the hope of treating AD and Huntington’s disease. She said the study found that rats, when treated with a peptide inhibitor, showed a 50% recovery of memory function, depending on tests such as navigation mazes.

Impact of Alzheimer’s disease

AD is a disease associated with aging that results in the death of stem cells, resulting in memory loss and cognitive impairment.

The numbers surrounding the disease are staggering – more than 5.7 million people have AD, and this group is estimated to reach 14 million by 2050, according to the Alzheimer’s Association. That figure is expected to reach 16 million by 2050. The annual out-of-pocket cost of Alzheimer’s disease exceeds $ 250 billion.

Understanding Pathology

Risk factors that contribute to AD include vascular disease that affects the heart and blood vessels. While others dangers well-known aging, for example — others, such as brain cholesterol, play an important role in understanding how the disease develops.

Brain cells communicate through cholesterol-rich cell membranes, a process that occurs naturally and is essential for healthy brain function. Studies show that the brain contains 23-25% of the body’s cholesterol.

“Cholesterol accumulates in the brain and causes damage to the neuron – it has long been recognized to play a role in Alzheimer’s disease,” Qi said. “However, what causes cholesterol buildup in the brain remains unclear and may take the answers.”

Study

The paper is the result of more than five years of research into the role of cholesterol in the brain and its relationship to AD.

Researchers set out to address two key questions:

  • What role does cholesterol play in the disease?
  • How can this new approach be used for future treatment options?

Qi, the lead author of the paper, said the study was based on a protein molecule, ATAD3A. Little is known about how protein works in neurodegenerative diseases.

“In Huntington’s disease, ATAD3A cells become very strong and oligomerized (repetitive), which is the cause of the disease,” Qi said. “We worked together data scientists to see if ATAD3A also has a link to Alzheimer’s disease and, to our surprise, we found that genes are a major competitor associated with Alzheimer’s. “

From there, the researchers collected data through product analysis and found a mechanism that binds ATAD3A to brain cholesterol. The researchers found that once ATAD3A produced the same or similar components through a process called oligomerization, it suppressed a protein called CYP46A1. And the new protein prevents cholesterol from entering the brain, meaning it accumulates. Researchers have linked the collection brain cholesterol to disease progression in neurodegenerative diseases.

Findings

Evidence suggests that ATAD3A — particularly during oligomerization — may be involved in AD development.

With the potential target identified, Qi believes the next step to treatment lies in peptide inhibitors, which bind to ATAD3A and block it in action.

“Solutions treated with peptide have shown improved performance on memory testing,” Qi said. “They show increased memory capacity, hard work and intelligence and up to 50% recover from memory damage.”

This means that targeted ATAD3A oligomerization may slow the progression of Alzheimer’s disease, Qi said. Experimental testing is ongoing.


Cholesterol triggers the formation of Alzheimer’s plaque, according to a study


Learn more:
Yuanyuan Zhao et al, ATAD3A oligomerization improves neuropathology and cognitive impairment in Alzheimer’s disease models, Environmental communication (2022). DOI: 10.1038 / s41467-022-28769-9

hintThe study found a therapeutic target for Alzheimer’s disease, outlining strategies for reducing disease progression (2022, April 11) retrieved 11 April 2022 from https://medicalxpress.com/news/2022-04-therapeutic-alzheimer-disease- revealing-strategy. html

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