Dr. Magdalena Sastre graduated in Sciences and did her PhD in Biology and Health Sciences at the University of the Balearic Islands, Spain. She trained in Neuroscience in the USA (Cornell University and New York University) and in Germany (Universities of Munich, Bonn and Frankfurt).
She is interested in the molecular mechanisms whereby inflammation impacts on aging-related neuronal degeneration. During the last 20 years she has been investigating the effect of amyloid-ß (Aß) peptide in neuronal damage by exerting a neurotoxic and neuroinflammatory action and reducing neuronal survival. Her research is based on a multidisciplinary approach using molecular/cell biology, pharmacological, imaging and biochemical techniques to understand the regulation of amyloid precursor protein (APP) metabolism in relation to neuronal degeneration and eventual regeneration.
The projects that are currently carried out in her laboratory are related to the role of the activation of glial cells and neuroinflammation in neurodegeneration, particularly analysing the effects in the development of dementia. For that purpose, her team uses animal models of Alzheimer’s disease (AD) and they have also set up two animal models of traumatic brain injury (TBI), which it is known to accelerate the risk and onset of AD.
Her scientific contributions include the study of the intracellular signalling cascade of the amyloid precursor protein and how it affects its cleavage and the formation of amyloid-β peptide. In addition, she is exploring further treatments for dementia based on their anti-inflammatory and neuroprotective properties, particularly the peroxisome proliferator-activated receptor-γ (PPAR-γ) activators. During the past few years she has been studying the role of the PPARγ cofactors, in particular the coactivator PGC1α, showing that increased expression of the co-factor PGC1α using gene therapy leads to reduced AD pathology, improved memory and decreased neuronal loss (Katsouri et al, 2016).
et al., 2016, PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase in an Alzheimer’s disease model, Proceedings of the National Academy of Sciences of the United States of America, Vol:113, ISSN:0027-8424, Pages:12292-12297