A groundbreaking study from Johns Hopkins University suggests that more than 200 types of misfolded proteins, beyond the well-known A-beta and tau amyloids, may contribute to age-related cognitive decline. Published in Science Advances, the findings could open new avenues for treating Alzheimer’s and dementia, which affect millions of people over 65 worldwide.
Researchers studied 17 aging rats, comparing those with cognitive impairment to those with sharp mental function. By analyzing over 2,500 proteins in the hippocampus—the brain region critical for memory—they identified more than 200 proteins that misfolded only in impaired rats. These proteins, unlike amyloids, do not clump together but still disrupt brain function.
“Amyloids are big and easy to see, but our work shows they’re just the tip of the iceberg,” said lead researcher Stephen Fried, a protein scientist at Johns Hopkins. “Many misfolded proteins evade the cell’s cleanup system, potentially harming cognitive health.”
The study challenges the long-held focus on amyloids alone, suggesting a broader range of proteins may play a role in dementia. Next, the team will examine these proteins at the molecular level to understand how they evade cellular defenses.
“Understanding these mechanisms could lead to better treatments,” Fried added, emphasizing the urgency of addressing cognitive decline in aging populations.
This research marks a significant step toward uncovering the complex causes of Alzheimer’s and dementia, offering hope for future therapies.
Add comment