Publications by authors named "Marissa Calvano"
Article Synopsis
- Alzheimer's disease (AD) is characterized by protein aggregates, inflammation, and issues with blood vessels, including a damaged blood-brain barrier that allows harmful proteins like fibrinogen to enter the brain.
- Fibrinogen interacts negatively with amyloid-beta (Aβ) peptides, worsening blood flow and clotting issues associated with AD.
- Lecanemab, an FDA-approved treatment for AD, helps remove Aβ plaques and prevents negative interactions between Aβ and fibrinogen, potentially slowing disease progression.
Article Synopsis
- Alzheimer's disease (AD) is characterized by protein-rich brain inclusions, neuroinflammation, and problems with blood vessels, which includes a weakened blood-brain barrier that allows blood proteins like fibrinogen to enter the brain.
- Fibrinogen interacts negatively with the amyloid-beta (Aβ) peptide, worsening blood clotting issues and blood flow in AD.
- Lecanemab, an FDA-approved antibody for AD, shows potential to reduce Aβ levels and slow cognitive decline by blocking the harmful interaction between Aβ and fibrinogen, preventing further damage in the brain.
A possible mechanism for the enhanced toxicity of beta-amyloid protofibrils in Alzheimer's disease.
Proc Natl Acad Sci U S A
September 2023
Article Synopsis
- The amyloid-beta peptide (Aβ) plays a significant role in Alzheimer's disease (AD), with its protofibrils being identified as the most toxic form.
- A recently FDA-approved antibody called lecanemab targets these protofibrils, showing effectiveness in slowing AD progression.
- The study suggests that Aβ protofibrils activate the plasma contact system, leading to inflammation and vascular issues in AD, with lecanemab blocking this detrimental activation.
A dysregulated plasma contact system is involved in various pathological conditions, such as hereditary angioedema, Alzheimer disease, and sepsis. We previously showed that the 3E8 anti-high molecular weight kininogen (anti-HK) antibody blocks HK cleavage and bradykinin generation in human plasma ex vivo. Here, we show that 3E8 prevented not only HK cleavage but also factor XI (FXI) and prekallikrein (PK) activation by blocking their binding to HK in mouse plasma in vivo.
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