Present Institution:

I3S - Institute for Research and Innovation in Health

Location:

Porto PT

Career Status:

Faculty Academia
Professor
Assistant Professor
Research Assistant

Bio

I graduated in Biochemistry and soon started to develop research in the area I always wanted to investigate: Familial Amyloidotic Polyneuropathy (FAP)
contributing to understanding the mechanism of Transthyretin (TTR) amyloid formation
to the design of therapeutic approaches to FAP and identification of novel biomarkers in FAP. I got interested in other functions of TTR
such as its neuroprotective role in Alzheimer’s Disease (AD). A discovery consortium was established to screen and prioritize a list of small Molecular chaperones (SMCs)
all candidates as therapeutic agents for AD. The foundations of this project were my prior discoveries that
in AD
TTR is an unstable tetramer and that it is possible to improve the TTR/Aß interaction with these SMCs. Supervision of PhD
Master undergraduate students are also part of my activities
as well as teaching
both in undergraduate programs and in post-graduate formations
at the University of Porto. Finally
I have also been participating in different activities for the public
and high school students by offering 3 lab visits/per year and by hosting 2 students/per year in the lab
for 1 week
for project development
among others. Orcid: 0000-0003-2472-7055.

Interested in presenting:

Neurodegenerative disorders

Sample of a Science/Scholarship Abstract

15 December 2022 – Biomedicines (MDPI) 2022 webinars: Alzheimer’s Disease: the history of forgetting. Presentation: “Dissecting unexplored mechanisms underlying Transthyretin neuroprotection”. Isabel Cardoso 16-17 February 2021- FEUP- 1st Symposium on Alzheimer’s Disease: An Update on Pathology and Therapeutics. Dissecting unexplored mechanisms underlying Transthyretin neuroprotection and advancing towards a therapy for Alzheimer's Disease. Isabel Cardoso.

What type of talks have you presented in the past?

Transthyretin influences the cerebrovascular system in Alzheimer’s Disease – deciphering the underlying pathways Cerebrovascular dysfunction is common in Alzheimer's disease (AD)
often preceding many of the AD typical hallmarks. Transthyretin (TTR) is a recognized neuroprotective protein in AD
although diminished in the pathology. Here
we aimed to investigate the role of TTR in these vascular alterations and the effect of TTR tetrameric stabilization to improve its function and revert cerebrovascular dysfunction. 7 months AD/TTR+/− mice showed a ticker basement membrane (BM)
as assessed by immunohistochemistry for collagen IV
compared to AD/TTR+/+
both in the cortex and hippocampus. Vessel density was reduced in AD/TTR+/- only in the hippocampus
suggesting BM thickening precedes the decrease in vessel length. Mice treated with a TTR tetrameric stabilizer
Iododiflunisal
presented decreased BM thickness and increased vessel length
compared to controls. In vitro
TTR stimulated the expression of angiogenic markers VEGF
Ang-2
IL-6
and IL-8. Our findings show TTR has a direct impact on the vascular changes that occur in AD and might be used to revert vascular dysfunction.