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Mechanisms of protection and repair of the neurovascular unit in neurodegeneration.
The main target of our group is the neurovascular unit in health and disease of the Central Nervous System.
We focus our study on the mechanisms of protection and repair of the neurovascular unit in ictus, Alzheimer´s and tumoral progression with the aim of developing strategies in order to prevent or to slow down the progression of neurodegeneration.
The neurovascular unit dysfunction leads to ischemia and predisposes or exacerbates the development of high prevalent and impact socioeconomic diseases such as acute stroke (ictus) and chronic neurodegenerative diseases, particularly Alzheimer's, Parkinson's and dementia.
Our research project pursue a better understanding of the molecular mechanisms involved in protection and repair of the neurovascular unit with the aim to find effective therapies for the prevention and/or treatment of these diseases.
We carry out a multidisciplinary research on the involvement of the neurovascular unit in diseases affecting the nervous system, including stroke, brain tumors and Alzheimer's disease.
We undertook the study in rodent models by applying anatomical, histochemical, biochemical, and cellular and molecular biology techniques.
Experimental models are: i) ischemic stroke, conducted by permanent or temporary ligation of the middle cerebral artery, or using an intraluminal filament, ii) an orthotopic model for brain tumors, and iii) an Alzheimer´s disease genetic model, the double transgenic mice expressing the Swedish mutation of APP together with PS1 deleted in exon 9 (APPswe, PS1-dE9).
Our main goals are:
- Study of the role of AM and NO systems in cerebral ischemic pathology, particularly in ischemic stroke, and search for effective molecules capable of reducing the ischemic penumbra.
- Research into effective molecules capable of delaying or stopping the neurodegeneration underlying Alzheimer's disease.
- Search mechanisms to slow tumor progression: the use of nanoparticles (nanohyperthermia).
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