The most common form of CAA is characterized by Aβ deposition in cerebral blood vessels, making it the leading cause of lobar intracerebral hemorrhage (ICH) in the elderly. Recurrent ICH significantly increases mortality and disability. CAA is highly prevalent in AD patients, highlighting a strong pathological link between the two diseases. Several factors influence vascular versus parenchymal Aβ deposition, including peptide length, co-deposited proteins, and APOE genotype. Understanding these factors is crucial to uncovering the intersection between CAA and AD and their implications for treatment strategies. Currently, no effective therapeutic options exist for CAA, and a definitive diagnosis requires histopathological confirmation.

In this talk, Dr. Hernández-Guillamon will present the latest advances in CAA clinical diagnosis and biomarker discovery in biological fluids. She will highlight recent findings from her laboratory, including the identification of Milk Fat Globule-EGF Factor 8 (MFG-E8) as a novel biomarker for CAA and a potential therapeutic target. Additionally, she will explore the relationship between lipid metabolism and cerebral Aβ deposition, discussing recent experimental approaches involving non-invasive therapeutic strategies aimed at increasing the circulating levels of specific apolipoproteins to prevent the hemorrhagic burden in a transgenic mouse model of CAA. This presentation will provide insights into the intersection between CAA and AD, offering new perspectives on diagnostic and therapeutic advancements for this complex neurovascular disorder.