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中文Research Highlights
- Publish Date：2025-05-15
NYCU and NHRI Study Reveals New Hope for Alzheimer’s Treatment from a Surprising “Virus Warrior” Gene
The research team (from right: NHRI Director Dr. Shie-Liang Hsieh, NYCU Institute of Brain Science Associate Professor Han-Juo Cheng, and Ph.D. student Yu-Yi Lin).
Translated by Szu-Yung Huang
Edited by Chance Lai
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Edited by Chance Lai
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Can a gene once believed to fight only viral infections also hold the key to preventing memory loss in Alzheimer’s patients? In a groundbreaking discovery, researchers from National Yang Ming Chiao Tung University (NYCU) and Taiwan’s National Health Research Institutes (NHRI) have revealed that the immune gene CLEC5A plays a critical role in the progression of Alzheimer’s disease, rewriting the scientific community’s long-held understanding of dementia. Published in the prestigious Journal of Neuroinflammation, this breakthrough offers unprecedented insights into Alzheimer’s disease mechanisms and paves the way for new drug development.
CLEC5A – The Double-Edged Sword of Immunity
Traditionally, CLEC5A has been associated with viral defense, activating the immune system in response to diseases like dengue fever, Japanese encephalitis, influenza, and COVID-19. It has also been linked to the deadly "cytokine storm" phenomenon. However, in a surprising twist, a research team led by Associate Professor Han-Juo Cheng of NYCU's Institute of Brain Science and Dr. Shie-Liang Hsieh, Director of NHRI's Immunology Research Center, discovered that this gene also plays a pivotal role in Alzheimer's disease.
Using genetic engineering techniques, the team bred Alzheimer's model mice that lacked the CLEC5A gene and compared them with normal Alzheimer's mice. The results were astonishing: mice without the CLEC5A gene performed significantly better in memory and learning tests. They showed a marked reduction in harmful β-amyloid plaque accumulation—a hallmark of Alzheimer's pathology.
Blocking the Gene to Restore Brain Defense
Professor Cheng explained that microglia—the brain’s resident immune cells—become hyperactive in response to abnormal β-amyloid buildup, mistakenly attacking healthy neurons and accelerating disease progression. However, when CLEC5A was removed, not only did microglial inflammation decrease, but their ability to clear β-amyloid improved dramatically, slowing the progression of brain degeneration.
CLEC5A – The Double-Edged Sword of Immunity
Traditionally, CLEC5A has been associated with viral defense, activating the immune system in response to diseases like dengue fever, Japanese encephalitis, influenza, and COVID-19. It has also been linked to the deadly "cytokine storm" phenomenon. However, in a surprising twist, a research team led by Associate Professor Han-Juo Cheng of NYCU's Institute of Brain Science and Dr. Shie-Liang Hsieh, Director of NHRI's Immunology Research Center, discovered that this gene also plays a pivotal role in Alzheimer's disease.
Using genetic engineering techniques, the team bred Alzheimer's model mice that lacked the CLEC5A gene and compared them with normal Alzheimer's mice. The results were astonishing: mice without the CLEC5A gene performed significantly better in memory and learning tests. They showed a marked reduction in harmful β-amyloid plaque accumulation—a hallmark of Alzheimer's pathology.
Blocking the Gene to Restore Brain Defense
Professor Cheng explained that microglia—the brain’s resident immune cells—become hyperactive in response to abnormal β-amyloid buildup, mistakenly attacking healthy neurons and accelerating disease progression. However, when CLEC5A was removed, not only did microglial inflammation decrease, but their ability to clear β-amyloid improved dramatically, slowing the progression of brain degeneration.
This discovery positions CLEC5A as a promising new therapeutic target for Alzheimer’s. By designing drugs to block this gene’s protein function, scientists believe they may open a new front in the battle against dementia.
An Accidental Breakthrough from the “Virus Warrior” Gene
“It started as a hunch without solid evidence,” admitted Dr. Hsieh, who previously identified CLEC5A as a key factor in severe dengue and Japanese encephalitis cases. Initially, the team was uncertain whether this virus-related gene could also be implicated in Alzheimer’s.
However, further research revealed that CLEC5A doesn’t just recognize viruses—it’s also involved in autoimmune diseases like lupus, raising suspicions that it might also mistakenly attack the brain’s nerve cells.
This landmark study also credits NYCU doctoral students Yu-Yi Lin and Wen-Han Chang for their critical contributions. The findings, now officially published in the Journal of Neuroinflammation, have drawn significant attention from the international scientific community.
As Alzheimer’s cases rise globally, this breakthrough led by Taiwan’s scientific teams not only offers a fresh perspective on the disease’s origins but also points to an entirely new direction for drug development. Shortly, targeted therapies against CLEC5A could offer countless families a new beacon of hope in the fight against memory loss.
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