In the search for a treatment for Alzheimer’s, a complex and devastating disease, researchers have long struggled to find effective therapies. The recent FDA approval of lecanemab gives hope.
This antibody treatment targets a specific form of the amyloid beta peptide (Aβ), which is thought to be one of the main causes of Alzheimer’s.
A new study from Rockefeller University examines lecanemab’s mechanism of action and may offer new avenues to treat not only Alzheimer’s but a host of other diseases.
Alzheimer’s is a global health crisis with rising case numbers. Current therapies such as aducanumab have significant side effects such as amyloid-related imaging abnormalities (ARIA), which include edema and bleeding.
However, lecanemab had significantly fewer ARIA cases, raising questions about its mechanism of action.
The mechanism behind lecanemab
The study, led by Erin Norris, focuses on protofibrils, a specific type of Aβ clump. Norris and her team found that these protofibrils activate the plasma contact system, a backup for the body’s primary coagulation system.
Activation of this system has been linked to Alzheimer’s-associated cerebrovascular abnormalities such as bleeding and decreased blood flow.
By targeting these protofibrils, lecanemab disrupts this activation process, which likely explains its lower side effect profile.
The Promise of a New Therapy – 3E8
The study opens up new treatment options.
Norris and Sidney Strickland, co-lead authors of the study, developed an antibody called 3E8 that blocks activation of the plasma contact system by targeting high molecular weight kininogen (HK).
This treatment could be used alone or in conjunction with anti-Aβ therapies such as lecanemab, potentially eliminating ARIA as a side effect.
The researchers also note that contact system dysregulation is common in other diseases such as COVID, sickle cell anemia, sepsis and cancer.
This means that therapies like 3E8 could have far-reaching applications beyond Alzheimer’s disease.
The research provides crucial insights into how lecanemab works and explains the lower rate of side effects compared to other Alzheimer’s therapies.
3E8 also opens a potential new therapeutic avenue that could either complement existing treatments or offer a new strategy to combat Alzheimer’s and other diseases in which the plasma contact system is dysregulated.
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The study was published in the PNAS.
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