Recently, a research team from McGovern Medical School of Texas Jianzhong Science Center revealed an unknown pattern of aging in brain cells, which can be used as a test indicator to diagnose late decades before the onset of dementia symptoms. Hairstyle Alzheimer's disease (AD).
Late-onset Alzheimer's disease usually develops at the age of 65. When there are symptoms such as memory loss and language deterioration, the brain has lost a lot of neurons. The McGovern Medical School team believes that a sudden aging of the 40-year-old brain may be the best time to look for biomarkers (predicting Alzheimer's disease) that can be diagnosed and intervened before brain damage.
Discover key proteins that control aging
The new discovery, published in the Nature issue of Translational Psychiatry, involves a key protein, interleukin 33 (IL33), a protein that activates the body's repair mechanisms and is expressed in large amounts in the brain to restore neurons to health.
Professor Yahuan Lou and the team first noticed the function of IL33 when studying mouse ovarian function defects. They found that when IL33 was removed, the ovarian contraction rate was significantly faster than normal. So, if the brain lacks IL33, what effect will it have?
In search of answers, Yahuan Lou team and psychiatry professor Joao De Quevedo and Mitchell Center Dementia Research Assistant Professor Ines Moreno-Gonzalez found that in the absence of IL33, middle-aged mice (equivalent to human 40 years old) brain neurons Suddenly turned to aging, degeneration, until suffering from Alzheimer's disease.
"We believe that aging is a process of gradual development. However, these brain cells in the experiment are not 'conventional'," stressed Yahuan Lou, a journal communication author and biology professor.
Professor Joao De Quevedo (left) and Professor Yahuan Lou (right)
Provide new ideas for treating dementia
A research team in Singapore conducted an experiment to simulate familial early-onset Alzheimer's disease with a mouse model. When they injected IL33 protein into dementia mice, the age spots in the brain decreased. However, they don't know why. “Now we have found the reason,†explains Professor Yahuan Lou.
Moreover, artificial injection of IL33 protein only temporarily slows down the symptoms and does not completely cure the disease. This effect lasts for about 2 weeks (equivalent to a few months of humans). Yahuan Lou believes that a way to stimulate the brain to supplement IL33 should be found in order to achieve the true treatment expectations.
There are many pathogenic factors in Alzheimer's disease, including neuroinflammation, abnormal aging, smoking, and infection. The lack of IL33 is a new idea that deserves to be explored and tapped into potential.
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