New Understanding of Alzheimer's Could Transform Treatment Approach

Researchers at Emory University have challenged our basic understanding of how Alzheimer's disease damages the brain. Their findings, published in Cell Reports Medicine, point to a different mechanism than previously thought.

Key findings:

• Amyloid beta plaques act as scaffolds that collect other proteins
• These additional proteins may cause brain cell damage, not the amyloid itself
• Research team identified over 20 proteins that build up with amyloid
• Two specific proteins, midkine and pleiotrophin, speed up amyloid buildup

What this means for treatment:

• Current therapies target amyloid beta alone
• New research suggests targeting other proteins could work better
• Opens up fresh treatment possibilities for other diseases involving protein buildup
• Could explain why previous treatments have failed in trials

The research team used advanced technology to analyze more than 8,000 proteins in both human and mouse brains with Alzheimer's. They focused on proteins showing the biggest increases around amyloid buildups.

Dr. Todd Golde, who led the study at Emory's Center for Neurodegenerative Disease, notes that these additional proteins might be the real culprits behind brain damage, not just the amyloid deposits themselves.

Next steps:

• Further research to identify more proteins involved
• Development of new diagnostic markers
• Testing of treatments targeting these newly found proteins
• Possible applications to 30+ other protein-buildup disorders

This shift in understanding Alzheimer's development offers hope for more effective treatments of this brain disease that has resisted previous therapeutic approaches.

[Research supported by National Institutes of Health and published in Cell Reports Medicine]

https://news.emory.edu/stories/2024/08/hs_alzheimers_12_08_2024/story.html

‍