Researchers have uncovered a promising new approach that could one day help treat Alzheimer’s disease by helping the brain remove harmful proteins.
The study, led by scientists at the USC Stem Cell research center, focuses on a natural cleaning process inside brain cells instead of blocking important brain chemicals. The findings were published in the journal Neuron.
Alzheimer’s disease is the most common cause of dementia and affects millions of people around the world. It slowly damages memory, thinking, and the ability to carry out everyday tasks. Although current medicines may temporarily ease symptoms for some people, they cannot stop the disease from getting worse.
One of the main features of Alzheimer’s disease is the buildup of abnormal proteins inside the brain. One of these proteins is called tau. When too much damaged tau collects inside nerve cells, it interferes with their normal function, eventually leading to cell death and memory loss.
Scientists have known that another brain chemical, called glutamate, plays an important role in this process. Glutamate is essential for learning, memory, and communication between brain cells. However, too much glutamate activity can trigger harmful changes that encourage toxic tau to build up.
Simply reducing glutamate is not a practical treatment because the chemical is vital for normal brain function. Lowering glutamate too much could lead to serious side effects, including memory problems, movement difficulties, and even loss of consciousness. Instead, the research team searched for a safer way to protect brain cells.
To do this, the scientists studied tiny laboratory-grown brain organoids created from human stem cells. These miniature brain models were made using cells from both healthy people and patients with tau-related brain diseases. They also studied mice carrying a genetic change known to cause a form of dementia.
When the researchers exposed these brain models to glutamate, they found that toxic tau quickly accumulated and nerve cells began to die, especially in tissue carrying disease-related changes. The team then searched for genes that became active during this process. One gene, called KCTD20, stood out as playing a major role.
When the researchers reduced the activity of KCTD20, the results were encouraging. Tau buildup fell sharply, and many nerve cells remained healthy despite exposure to glutamate. Further experiments showed that blocking this gene activated lysosomes, tiny structures inside cells that act like recycling and waste-disposal centers by breaking down unwanted material.
The activated lysosomes surrounded the harmful tau proteins and removed them from the cells, allowing the brain’s natural cleaning system to work more effectively. Rather than preventing tau from forming, this strategy helped the brain get rid of the toxic protein before it could cause more damage.
Although the work is still at an early stage and has not yet been tested as a treatment in people, the discovery offers an exciting new direction for Alzheimer’s research. Future medicines that target KCTD20 or strengthen lysosome activity may help slow the progression of Alzheimer’s disease and other forms of dementia while avoiding the side effects of altering glutamate itself.
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