Icahn Mount Sinai researchers find PLXNB1, a hub gene predicted to drive a gene subnetwork causally linked to human AD, is upregulated in reactive astrocytes surrounding amyloid plaques. Credit: Bin Zhang, PhD, Icahn Mount Sinai
Key points:
- Researchers used complex data network models to examine the plexin-B1 pathway’s role in clearing amyloid plaques in the brain.
- The team found that reactive astrocytes played a major role in the clearing process by controlling the spacing around amyloid plaques.
- These findings highlight new ways to slow down or halt disease progression, which opens the door to new treatment strategies.
Researchers have made a significant breakthrough in Alzheimer’s disease research by developing a new approach to slow down or even halt disease progression. The findings, published in Nature Neuroscience, demonstrate a new role for reactive astrocytes and the plexin-B1 protein.
Researchers analyzed complex data comparing healthy individuals to those with Alzheimer’s disease. Using this data, they focused on manipulating the plexin-B1 protein to enhance the brain’s ability to clear amyloid plaques. They found that reactive astrocytes – a type of brain cell that is activated in response to injury or disease – played a key role in the clearing process as they control the spacing around amyloid plaques.
“Our study opens new pathways for Alzheimer’s research, emphasizing the importance of cellular interactions in developing neurodegenerative disease treatments,” explained study lead author Hongyan Zou, professor at Icahn Mount Sinai.
This study represents a major step forward in the validation of multiscale gene network models of Alzheimer’s disease. It both confirms a major model prediction and advances the knowledge needed to develop novel therapeutics. The research team believes that showing a critical role for plexin-B1 in Alzheimer’s disease will help the development of targeted therapies to disrupt disease progression.
While these findings are a significant advance in the fight against Alzheimer’s, researchers note that more research is needed to translate their work into treatment for human patients.
“Our ultimate goal is to development treatments that can prevent or slow down Alzheimer’s progress,” said study lead author Bin Zhang, progress at Icahn Mount Sinai.