New research from Emory University challenges current ideas about Alzheimer’s origins. Scientists at the Goizueta Brain Health Institute found evidence suggesting a different cause of Alzheimer’s.
In their August 9 paper in Cell Reports Medicine, Todd E. Golde and Yona Levites explain that amyloid beta deposits in the brain might act as a scaffold, attracting other proteins. These proteins, rather than the amyloid itself, could be responsible for brain cell damage in Alzheimer’s patients.
In Alzheimer’s patients, amyloid proteins build up into sticky plaques that disrupt brain function and lead to cognitive decline. The exact process needed to be clarified. The standard theory is that amyloid beta buildup harms brain cells by disrupting communication and activating immune cells.
However, a new study by Todd Golde and Yona Levites from Emory University suggests a different role for amyloid beta. Using advanced technology, they analyzed over 8,000 proteins in both human and mouse brains with Alzheimer’s. They found more than 20 proteins that accumulate with amyloid beta, which may play a vital role in the disease. Their research continues to explore this discovery.
After identifying new proteins linked to Alzheimer’s, the researchers wanted to see if these proteins were just markers or if they influenced the disease. They found that two proteins, midkine, and pleiotrophin, speed up amyloid buildup in lab tests and mice. This suggests these proteins may contribute to brain damage, offering potential new targets for Alzheimer’s treatment.
Alzheimer’s has been studied for over a century, but finding a cure has been difficult. The disease is complex, and past treatments have often failed. This new research challenges the old idea that amyloid buildup alone causes Alzheimer’s, suggesting that other proteins may also play a role. This could lead to new treatments not only for Alzheimer’s but also for other diseases involving amyloid buildup.
Journal reference:
- Yona Levites, Eric B. Dammer et al., Integrative proteomics identifies a conserved Aβ amyloid responsome, novel plaque proteins, and pathology modifiers in Alzheimer’s disease. Cell Reports Medicine. DOI: 10.1016/j.xcrm.2024.101669.
