Scientists have long known that the Alzheimer’s brain often features abnormal plaques and tangles, and recent studies have highlighted the role that the brain’s vascular system plays in disease progression.
Scientists have long known that the Alzheimer’s brain often features abnormal plaques and tangles, and recent studies have highlighted the role that the brain’s vascular system plays in disease progression. But for decades, this knowledge has failed to translate into fully effective treatments. The lack of progress is largely due to the fact that, despite landmark findings, the precise pathway of neurodegeneration is still unclear.
Now, new research demonstrates that when Aβ binds to fibrinogen—a major blood protein—it forms abnormal clots that are resistant to degradation. These clots are linked to vascular damage and inflammation, and even small amounts of this complex appear to trigger early Alzheimer’s pathologies, such as synapse loss, neuroinflammation, and blood–brain barrier disruption. The findings strengthen the evidence that vascular disease contributes to neurodegeneration and provide hope for AD patients in the form of a promising new drug target: Aβ/fibrinogen complexes.
“It takes a larger amount of Aβ or fibrinogen alone to cause serious damage in the Alzheimer’s brain,” says Erin Norris, research associate professor in the laboratory of Sidney Strickland at Rockefeller. “But when the two complex together, you only need very small amounts of each to cause damage. There’s a synergistic effect with Aβ and fibrinogen.”
Read More: Rockefeller University
Photo Credit: geralt via Pixabay
