I am a neuroscientist with a strong background in neurodegenerative diseases, initially focusing on Alzheimer’s and amyloidosis in diagnosis and treatment strategies. In 2019, I expanded my research to multiple sclerosis (MS) and traumatic brain injury (TBI) to explore the interplay between vascular dysfunction, inflammation, and neurodegeneration. My goal is to identify therapeutic targets to halt neuroaxonal loss, bridging fundamental research with clinical applications. Using large post-mortem tissue cohorts, -omics strategies and iPSC-derived co-cultures, we identified fibrinogen as a marker of blood-brain barrier dysfunction and DAMPs proteins as drivers of chronic inflammation in MS. We also found that iron accumulates along a lumbar-to-cervical gradient, mirroring MS progression. In TBI, we study how vascular damage drives amyloid tau pathology using a large cohort from over 3,000 veterans. A major focus is the role of amyloids and Nurr1 in MS. We uncovered a distinct amyloid landscape, challenging the belief that amyloidosis is absent in MS. We also identified Nurr1 as a promising target to protect against neuroaxonal loss, inflammation, and demyelination. At the core of my research lies a key question: What comes first—vascular dysfunction, neurodegeneration, or inflammation? Perhaps, like the chicken-and-egg dilemma, they emerge together. Understanding this may unlock new therapeutic strategies.