OUR PARTNERS

The essence of our Astromad project

We are a consortium of institutions, universities and research groups working together to
achieve a deeper understanding of Alexander’s disease

  • PI and coordinator: Dolores Pérez-Sala

  • Department of Structural and Chemical Biology. Centro de Investigaciones
    Biológicas Margarita Salas, CSIC, Madrid, Spain

The posttranslational modification of proteins is a key mechanism for the regulation of their biological activity. We are interested in the study of the posttranslational modification of proteins in molecular pathophysiology and in the mechanisms of drug action.

We devote special attention to protein lipoxidation and its impact on the cytoskeletal proteins of the intermediate filament family in basic mechanisms and in disease, and, in particular, to the importance of GFAP lipoxidation in Alexander disease.

  • PI: Elly Hol

  • Department of Translational Neuroscience
    Brain Center UMC, Utrecht, The Netherlands

In Elly Hol’s group we focus our research on the cell and molecular biology of astrocytes and adult neural stem cells (neurogenic astrocytes) in health and disease.

Our work covers various aspects including neurodegeneration, stroke, autism, schizophrenia, neural stem cells and brain organoids, reactive astrocytes and GFAP.

  • PI: Milos Pekny

  • Laboratory of Astrocyte Biology and CNS Regeneration. Center for Brain Repair
    Department of Clinical Neuroscience
    Institute of Neuroscience and Physiology
    Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

Our laboratory focuses on the development of novel strategies
for brain repair and regeneration. We previously showed that reactive astrocytes are key players in stroke, neurodegeneration and disease-triggered neural plasticity responses.

By employing innovative technologies, including transgenic models, state-of-the-art imaging technologies, advanced transcriptomics and clinical material, we aim to determine the specific roles of astrocytes in ischemic and hemorrhagic stroke, post-stroke plasticity and in neurodegeneration in order to develop stroke therapies that will enhance brain plasticity and promote functional recovery through the modulation of astrocytes.

  • PI: Michael J. Davies

  • Department of Biomedical Science, University of Copenhagen, Denmark

Our group works to understand the mechanisms of protein modification by reactive species (radicals, two-electron oxidants, glycation reactions), the biological consequences of such reactions, and the development of methods to quantify protein damage in disease with a particular emphasis on cardiovascular pathologies.

The Protein Oxidation group is also very interested in peroxidase enzymes (particularly myeloperoxidase), EPR spectroscopy for the detection of transient radicals, the kinetics of oxidant reactions, extracellular matrix damage and the development of antioxidants and inhibitors of oxidant formation.

  • PI: Mariona Jové

  • Institut de Recerça Biomèdica de Lleida,
    Lleida, Spain

The overall goal of our investigations concerned the role of metabolism and oxidative stress (including free radical chemistry, redox biology and antioxidants) in the aging process and age-associated diseases.

We have investigated the role of metabolism and oxidative stress in animal models (vertebrates and invertebrates) and humans in which aging rate and longevity are different or are experimentally modified (e.g. caloric restriction, methionine restriction, and genetic manipulations) or pathologically affected (e.g. metabolic diseases, cardiovascular disease, cancer, neurodegenerative diseases).

If the aging process could be slowed or even reverted the incidence of age-related diseases would diminish significantly.

The Protein Oxidation group is also very interested in peroxidase enzymes (particularly myeloperoxidase), EPR spectroscopy for the detection of transient radicals, the kinetics of oxidant reactions, extracellular matrix damage and the development of antioxidants and inhibitors of oxidant formation.