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Introduction: A new study suggests that the accumulation of a key protein molecule within the brain is key to triggering Alzheimer's, and the use of peptide inhibitors as therapeutic targets plays an important role in Alzheimer's treatment. The study found that, based on tests such as maze navigation, mice recovered 50% of their memory function after receiving peptide inhibitor treatment.
Alzheimer's, the most common form of dementia that causes memory loss and memory impairment, has shown a high incidence in the near term, with the World Health Organization predicting that the number of people living with Alzheimer's will increase by millions each year. Although scientists have been working on it for decades, no cure has yet been found.
Risk factors that lead to Alzheimer's include vascular diseases that affect the heart and blood vessels. Although some risk factors are well known, such as aging. But other risk factors, such as brain cholesterol, play an important role in disease progression.
Brain cells communicate through cholesterol-rich membranes, a naturally occurring process that is essential for healthy brain function. Studies have shown that the brain contains 23-25% of the body's cholesterol.
Cholesterol accumulates in the brain and causes damage to neurons, and it has long been thought that it plays a role in the pathology of Alzheimer's disease, and the cause of cholesterol accumulation in the brain is unknown, but researchers have made breakthroughs in protein molecules.
Recently, researchers at the Case Western Reserve University School of Medicine published a study in the journal Nature, which said that a key protein molecule, ATAD3A, plays an important role in the accumulation of cholesterol in the brain, which in turn triggers the progression of Alzheimer's disease.
The study focused on the protein-coding gene ATAD3A. It is unclear how this protein plays a role in neurodegenerative diseases.
In Huntington's disease, the ATAD3A molecule becomes hyperactive and is oligomerized (repeated), which is what causes the disease," ATAD3A was found to be associated with the development of Alzheimer's disease.
The researchers collected data by analyzing the model and discovered a pathway linking ATAD3A to brain cholesterol. The researchers found that once ATAD3A forms repetitively similar or identical parts through a process called oligomerization, it inhibits another protein called CYP46A1. The new protein then prevents cholesterol from being metabolized in the brain, which means it accumulates. Researchers have linked the accumulation of brain cholesterol to disease progression in neurodegenerative diseases.
The models that the scientists tried to treat with peptides performed better on memory tests, showing stronger memory, stronger cognitive activity, and up to 50 percent recovery from memory impairment. ”
This means that targeting ATAD3A oligomerization may slow the progression of Alzheimer's disease, and further testing is underway.
Reference URL: https://www-sciencedaily-com.translate.goog/releases/2022/04/220411125401.htm?_x_tr_sl=en&_x_tr_tl=zh-CN&_x_tr_hl=zh-CN&_x_tr_pto=sc