Site icon Cerebral Amyloid Angiopathy (CAA)

Rage receptors, Taxifolin, Immunotherapy, Cilostazol-Taxifolin, and ApoA-1 as therapeutic targets for CAA

This summary of potential therapeutic targets for treating cerebral amyloid angiopathy is drawn primarily from an important review article, “Models of cerebral amyloid angiopathy-related intracerebral hemorrhage,” published by Sebastian, Vargas-George and Kunjan, R. Dave in “Brain Hemorrhages, Volume 3, Issue 4, December 2022, Pages 189-199.
Here is a link to the complete article:

Editors note: This summary was prepared in part with ChatGPT.

The article discusses potential therapeutic targets for the treatment of Cerebral Amyloid Angiopathy (CAA), a condition characterized by the accumulation of amyloid proteins in the brain’s blood vessels. Currently, there is no proven therapy for CAA, and most treatments focus on preventing the risk of spontaneous intracerebral hemorrhage (sICH).

RAGE (receptor for advanced glycation end-products). RAGE is expressed in various cell types involved in the immune-inflammation response. Studies suggest that RAGE may mediate the transport of amyloid-beta (Aβ) into the brain, making it a possible intervention point. Blocking RAGE has been shown to reduce reactive oxygen species (ROS) generation.

Editor’s note: This research interest in RAGE suggests that red meat, high-fat foods, and highly processed foods (and of course sugar) that increase advanced glycation endproducts may contribute to CAA. This may explain why some professionals recommend a Mediterranean diet for dealing with CAA.

Taxifolin. A flavonoid, taxifolin is another promising therapeutic approach for CAA. It has been found to disassemble Aβ and inhibit its assembly while restoring cerebrovascular reactivity in animal models of CAA. Editors note: We have recently posted on the potential of Taxifolin:

Immunotherapy for CAA. Additionally, international efforts are underway to revise diagnostic criteria and explore immunotherapy for CAA. Clinical trials are investigating drugs like ponezumab, a novel monoclonal antibody against Aβ1–40, and (R)-1–6-[(R)-2-carboxy-pyrrolidin-1-yl]-6-oxo-hexanoyl]pyrroli-dine-2-carboxylic acid (CPHPC). Editors note: A clinical trial of ponezumab failed to show convincing benefits.

Cilostazol and its interaction with taxifolin. The article also mentions the potential of drugs like cilostazol and their interaction with taxifolin for novel therapies. (It is possible that taxifolin may be more effective when combined with cilostazol.)

ApoA-1 and reconstructed HDL. Another approach involves Aβ-binding proteins like ApoA-I and reconstructed HDL (rHDL), which have shown promise in preventing Aβ accumulation and reducing inflammation.

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