Name: | Isabel dos Santos Cardoso |
Sigla: | ISC |
Estado: | Active |
961A-34D6-D5B6 | |
K-3903-2013 | |
6701390815 |
Email Institucional: | idcardoso |
|
I graduated in Biochemistry and pursued research on Familial Amyloidotic Polyneuropathy (FAP). My 2002 PhD, including work in Canada and Switzerland, contributed to understanding Transthyretin (TTR) amyloid formation and FAP therapies. With 20+ years of experience in TTR pathophysiology, I specialize in proteinopathies like FAP, Alzheimer’s, and Parkinson’s, focusing on preclinical Alzheimer’s Disease (AD) neurobiology, neurodegenerative models, and endothelial and neuronal cell systems, including hippocampal neurons.
I got interested in studying other functions of TTR, such as its neuroprotective role in AD, securing my first FCT-financed project in 2005, and contributing to my scientific independence. My team gained additional interests, including studying factors that modulate neurodegenerative diseases, understanding communication across brain barriers, and identifying common denominators in proteinopathies. I engaged in 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 of which are 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/Aβ interaction with these SMCs. Another FCT-approved project is dedicated to: a) exploring the TTR effect in key brain processes that are dysregulated in AD, b) finding correlations between TTR and clinical data from AD patients to explore TTR as a biomarker, to translate knowledge, c) validating in vivo de action of the best SMCs.
The last years were also dedicated to unraveling new functions of TTR, such as its angiogenic potential and involvement in glucose metabolism, fostering interest in the role of TTR in diabetes, particularly T1D, in which TTR is decreased.
Overall, my publishing record produced over 3300 citations and an H-index=32.