Agnieszka Rybak-Wolf wins Alzheimer‘s research grant

How do the ApoE4 gene variant and the herpes simplex virus work together to increase the risk of developing Alzheimer’s disease? Agnieszka Rybak-Wolf has been awarded a grant from Stiftung Alzheimer Initiative to study the molecular interaction between the two risk factors.

Dr. Agnieszka Rybak-Wolf, a Group Leader of the Organoids lab at the Max Delbrück Center in Berlin, has been awarded a 200,000 euro research grant from the Stiftung Alzheimer Initiative to investigate the early molecular mechanisms that may drive Alzheimer’s disease.

 

"My goal is to uncover the gene-environment interactions that trigger the earliest disease-associated processes", says Agnieszka Rybak-Wolf, Group Leader of the Organoids lab.

The grant will fund a three-year study on how the herpes simplex virus type 1 (HSV-1) interacts with a well-known genetic risk factor for Alzheimer’s, the ApoE4 gene variant. “We still do not fully understand why some people develop Alzheimer’s while others remain healthy despite similar risk factors,” Rybak-Wolf says. “My goal is to uncover the gene-environment interactions that trigger the earliest disease-associated processes.”

Around 95 percent of Alzheimer’s cases are sporadic, meaning they are not caused by inherited mutations but by a complex interplay of genes and environmental influences. Previous studies have shown that both ApoE4 and HSV-1 independently increase Alzheimer’s risk. However, people who carry ApoE4 and harbor a latent HSV-1 infection appear to have an even higher risk of developing the disease, yet the reasons for this remain unclear.

Rybak-Wolf aims to address this knowledge gap by using advanced human brain organoids ­­– miniature brain models grown from stem cells ­– to study what happens when brain cells with different ApoE variants are exposed to HSV-1. By analyzing the interactions on a molecular level and comparing them to patient samples, Rybak-Wolf hopes to identify early cellular warning signals and potential therapeutic targets.

The long-term goal is to shift treatment toward prevention. Her work could help lay the groundwork for new strategies to stop the disease before irreversible brain damage occurs.

 

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