"New Breakthrough in Alzheimer's Disease Research: Reversing Cognitive Decline with Peptides"

2023-04-16 02:08:00

A woman with Alzheimer’s disease eats lunch in the cafeteria of a nursing home in Saint-Quilin, eastern France, October 18, 2016. (Credit: PATRICK HERTZOG/AFP via Getty Images)

[See China, April 16, 2023]Alzheimer’s disease is commonly known as senile dementia. If someone in the family suffers from the disease, it will definitely have a great impact on a family. A major new breakthrough in science at the Massachusetts Institute of Technology (MIT) has revealed a new way to reverse Alzheimer’s disease with dramatic results.

Researchers have used peptides, also known as peptides, to interfere with enzymes that are normally overactive in the brains of Alzheimer’s patients,media reported. The compound stops an enzyme called CDK5 from becoming overactive, which can damage nerves and lead to cognitive decline.

Cai Lihui, a neuroscientist at the Massachusetts Institute of Technology of American descent, said that they found that the effect of this peptide is very significant. It has shown great effects in reducing neurodegenerative diseases, neuritis and other reactions, and in rescuing behavioral defects.

Are brain waves the secret to treating Alzheimer’s? | Li-Huei Tsai https://t.co/bZoN83gmfh pic.twitter.com/AtIalDqkPr

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The researchers hope their findings will lead to future studies of new drugs that could reverse Alzheimer’s disease. After further experiments, the researchers are optimistic that the peptide could eventually be used to treat Alzheimer’s and other dementia-related diseases.

Research published in the Proceedings of the National Academy of Sciences (PNAS) shows that when researchers tried to treat mice with Alzheimer’s disease with hyperactive CDK5, the peptide reduced their DNA damage, as well as neuroinflammation and neuropathy. element deficiency.

In addition, the researchers also tried to treat Alzheimer’s mice with Tau protein mutations with peptides. After treatment, the mutant Tao protein and neuronal deficits in these mice improved.

Alzheimer’s can be seen here

The eyes are the windows to the brain, said Christine Greer, director of medical education at the Institute for Neurodegenerative Diseases in Florida. The ophthalmologist said that you can see the nervous system directly from the fundus of the eye through the optic nerve and retina.

But how many can see signs of cognitive decline? The recent study looked at retinal and brain tissue samples from 86 people with varying degrees of mental decline over a 14-year period, according to Coroni, a professor of neurosurgery and biomedical sciences at Cedars-Sinai Medical Center in Los Angeles. Maya Koronyo-Hamaoui said they studied the link between the human retina and changes in brain and cognitive function.

In a study published in Acta Neuropathologica in February, the researchers compared samples from people with normal cognitive function to those with mild cognitive impairment and those with more advanced Alzheimer’s disease. It was found that whether it is Alzheimer’s disease patients or people whose cognitive ability has just declined, the β-amyloid protein that represents the key indicator of Alzheimer’s disease in their retinas has a significant increase.

The eyes are more than a window to the soul — they’re also a reflection of a person’s cognitive health. https://t.co/OMsyt4ISX3

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Research has been investigating why the eyes may be able to help diagnose Alzheimer’s disease before symptoms begin to appear. In fact, when memory and behavior are affected, Alzheimer’s disease is already very serious.

Memory loss begins decades before the first symptoms appear, says Richard Isaacson, a preventive Alzheimer’s neurologist also at the Florida Institute for Neurodegenerative Diseases. It has already started to appear in the brain. He said that if doctors can detect Alzheimer’s disease early, then people can choose a healthy lifestyle and control modifiable risk factors such as high blood pressure, high cholesterol and diabetes.

Responsible editor: Wang Jun

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