Fibres and textiles have been used as biomaterials for thousands of years, mainly as sutures and in dressings for wound care. Recently, it has become of increasing interest to use fibres as implantable materials to support the repair of damaged tissues and organs.

Investigation of the role of SIRT3 on mitochondrial function in E2-dependent resistance to oxidative stress both in vitro and in vivo.

Marie Curie Actions - Intra-European Fellowship for Career Development (IEF)

FP7-PEOPLE-2013-IEF

The main goal of the proposed research is to understand cancer stem cell (CSC) biology and to develop novel CSC-directed compounds. We will strive to elucidate the molecular basis of potassium ion transport involvement in CSC-phenotype acquisition, modulation and targeting and identify key mechanisms of these processes as novel biomarkers for improved diagnostic options and innovative mechanism-based therapeutic approaches.

Aberrant proteolytic cleavage of the amyloid precursor protein (APP) leading to increased formation/accumulation of β-amyloid peptide (Aβ) is considered a central event in the pahogenesis of Alzheimer's disease (AD). Although much has been known about the Aβ generation and its clearance, we still do not understand in great detail how Aβ metabolism is altered in the most common late-onset form of AD (LOAD) and what are the molecular trigger(s) that initiate these events. In this project we will test the hypothesis that cholesterol metabolism and membrane trafficking are tightly linked and that their dysregulation leads to Alzheimer's disease. 

Using a lysosomal disorder NPC as a model, the goal of this project is to investigate a role of lysosomal impairment on accumulation of amyloid-beta peptide (Abeta) and alpha-synuclein (a-syn), the two characteristic features in the pathogenesis of AD and PD.

The goal of this project was to further elucidate the mechanism/s of cholesterol-effect on the metabolism of APP and BACE1 – the two key proteins in the pathogenesis of Alzheimer's disease. Using biochemical, molecular biological and cell biological approaches we have tested the hypotheses that alterations in cholesterol metabolism (due to NPC1 dysfunction) contribute to accumulation of Abeta and the pathogenesis of AD by modulating endocytic trafficking of BACE1 and/or by modulating lysosomal/autophagic function.