Alzheimer’s disease is the most common form of dementia, affecting millions of people around the world. It slowly damages memory, thinking, and the ability to carry out everyday tasks.
As the disease becomes worse, people may struggle to recognize loved ones, communicate, or live independently. Although scientists have learned a great deal about Alzheimer’s over the past few decades, there is still no cure. Researchers continue to search for new ways to slow the disease or stop it before too much damage occurs.
A new study led by researchers at USC Stem Cell has uncovered a promising new strategy that could help the brain remove one of the harmful proteins linked to Alzheimer’s disease.
Instead of trying to block an important brain chemical, the scientists found a way to improve the brain’s own cleaning system so that it can remove toxic proteins more effectively. The findings were published in the journal Neuron.
One of the main proteins involved in Alzheimer’s disease is called tau. Under normal conditions, tau helps support the structure of nerve cells. However, in Alzheimer’s disease and several related brain disorders, tau changes its shape and begins to stick together.
These clumps of toxic tau damage nerve cells, interrupt communication between brain cells, and eventually lead to cell death. As more nerve cells are lost, memory and thinking abilities gradually decline.
The researchers focused on another important substance in the brain called glutamate. Glutamate is a natural chemical messenger that allows brain cells to communicate with each other.
It plays a vital role in learning, memory, movement, and many other brain functions. However, when glutamate activity becomes too high, it can place stress on brain cells and encourage the buildup of toxic tau proteins.
At first, reducing glutamate might sound like a simple solution. However, Dr. Justin Ichida from the Keck School of Medicine at USC explained that lowering glutamate directly is not a good treatment because the chemical is essential for normal brain function.
Reducing it too much could lead to serious side effects, including memory problems, movement difficulties, or even loss of consciousness.
Instead of blocking glutamate, the research team looked for another way to protect brain cells. They grew tiny brain-like structures in the laboratory using human stem cells. These miniature models, known as brain organoids, were created from both healthy people and patients with diseases caused by abnormal tau proteins.
When the organoids were exposed to glutamate, the diseased cells developed large amounts of toxic tau and many nerve cells died. The researchers also observed similar changes in mice carrying a gene mutation that causes a form of dementia.
The team then searched for genes that responded to glutamate and discovered one called KCTD20. When they reduced the activity of this gene in both the brain organoids and the mice, the results were striking. Toxic tau levels dropped, and the nerve cells remained much healthier even after exposure to glutamate.
Further experiments revealed how this happened. Reducing KCTD20 switched on tiny structures inside cells called lysosomes. Lysosomes act like the cell’s recycling and waste disposal system.
They collect damaged materials and unwanted proteins, break them down, and remove them from the cell. In this study, activated lysosomes surrounded the harmful tau proteins and cleared them away before they could cause as much damage.
This discovery is important because it suggests that helping the brain remove toxic tau may be safer than interfering with glutamate itself. By strengthening the brain’s natural cleaning system, future treatments may be able to slow the progression of Alzheimer’s disease while avoiding many unwanted side effects.
Dr. Jesse Lai, one of the study’s authors, said the findings show that improving tau clearance could become an important treatment strategy. Researcher Dr. Joshua Berlind added that the discovery may eventually lead to more targeted therapies for Alzheimer’s disease and other neurodegenerative disorders.
The work is still in the early stages, and much more research is needed before this approach can be tested in people. Scientists will need to develop medicines that safely reduce KCTD20 activity or increase the ability of lysosomes to remove harmful proteins. Even so, the results offer fresh hope that future treatments could slow the disease by helping brain cells protect themselves.
Every new discovery brings researchers one step closer to understanding Alzheimer’s disease. While there is still a long journey ahead, this study provides an exciting new direction that could one day improve the lives of millions of people living with dementia and their families.
If you care about Alzheimer’s disease, please read studies that bad lifestyle habits can cause Alzheimer’s disease, and strawberries can be good defence against Alzheimer’s.
For more information about brain health, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.
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