I graduated in Biochemistry and soon started to research in the area I always wanted to investigate: neurodegeneration, electing as PhD theme Familial Amyloidotic Polyneuropathy (FAP). My PhD thesis, which included work performed in Canada and in Switzerland, contributed to understanding the mechanism of TTR amyloid formation and to the design of therapeutic approaches to FAP (2002), further pursued and developed in the post-doc periods. The latter is directly linked to the studies that lead to the use of doxycycline and tauroursodeoxycholic acid as a treatment for TTR amyloidosis and was the basis of a phase II clinical trial (doi:10.3109/13506129.2012.678508). As an independent researcher, I developed an interest in studying other functions of TTR, such as its neuroprotective role in Alzheimer’s Disease (AD). I launched my career as an independent researcher in this topic with a first FCT-funded project as a PI granted in 2005. The area of AD allowed me to make use of the expertise gained before, putting my knowledge on amyloidosis and TTR biology to use in a completely different point of view. In January 2008, I started the Ciência 5- year contract, allowing me to assume, more robustly, scientific independence. By that time, I also hosted my 2nd Master's student (concluded in Dec 2009) and my first PhD student (concluded in Dec 2011), contributing to boosting my research. By then, we achieved the first results on the mechanism of TTR/Aß interaction and on the impact on Aß aggregation. The period of the FCT Investigator contract (June 2013-May 2018), can be described as the time for growth and opening of horizons. My team gained additional interests, including the study of factors that modulate neurodegenerative diseases, understanding communication across brain barriers, and identifying common denominators in protein aggregation disorders, such as FAP, AD, and Parkinson’s Disease (PD), among others. The time period 2015-2018 was dominated by the Marató project in which I engaged new national and international collaborations, with molecular imaging experts, medicinal chemists, and clinicians. Our discovery consortium has screened and prioritized a list of small Molecular chaperones (SMCs), all candidates as therapeutic agents for AD. The foundations of this project were my prior discoveries that established that, in AD, TTR is an unstable tetramer and that, in vitro, it is possible to improve the TTR/Aß interaction with these SMCs. The last years were dedicated to the unraveling of new functions of TTR, such as its angiogenic potential, and a recently FCT-approved project is dedicated to a) exploring the participation of TTR in key brain processes that are dysregulated in AD, b) finding correlations between TTR levels and stability, and data from patients (clinic, biochemical, genetic, imaging) to explore TTR as a biomarker (diagnostic, prognostic), to translate knowledge, c) validating in vivo de action of the best SMCs. Overall, my publishing record produced over 2900 citations and an H-index=31.