2005 - 2007

Mechanisms of neuroprotection in Alzheimer: Mitochondria and mitochondrial Ca2+ as targets of salicylate and estrogens.
Aspirin, NSAIDs and estrogen prevent neuron cell death and protect against Alzheimer and other neurodegenerative diseases but the action mechanism is unknown. Here we propose the hypothesis that these compounds protect neurons by preventing mitochondrial Ca2+ overload that precedes or disposes to cell death. To test this hypothesis we are using three different models of Alzheimer disease. This project is supported by Instituto de Salud Carlos III, Spanish Health Department (136.800 €). 2005 - 2007. IP Lucía Núñez. This project is being carried out in colaboration with clinical researchers Drs. Justino Gómez and Dr. Javier Blanco at the Valladolid University Hospital and The Benito Menni Hospital in Valladolid as well as the Intras Association.

Mechanisms of neuroprotection in Alzheimer: Mitochondria and mitochondrial Ca2+ as target of salicylate and estrogens.
Supported by Junta de Castilla y León. (14.300 €). 2005 - 2007. IP Lucía Núñez.

Pituitary physiopathology: cell plasticity and pituitary tumors.
Formerly, it was considered that the anterior pituitary was formed by 5 different cell types, each one secreting a different pituitary hormone. However, we have reported that a large population of anterior pituitary cells display a mixed phenotype. Here we propose to study the phenotype of multifunctional cells of the anterior pituitary in rat and mouse pituitaries as well as in human pituitary adenomas. This project is supported by Instituto de salud Carlos III, Spanish Health Department (130.000 €). 2004 – 2006. IP Carlos Villalobos This project is being carried out by basic researchers at IBGM as well as clinical researchers at the Valladolid University Hospitals including Neurosurgeons Dr. José Mª de Campos as well as Endocrinologists Dr. Daniel A. de Luis and Dr. Enrique Romero from the Valladolid University Institute of Endocrinology and Nutrition.

Cancer chemoprevention: mitochondrial Ca2+ as target of NSAIDs and new aspirins.
We propose to study the effects of several NSAIDs and new aspirins on mitochondrial control of Ca2+ signals involved in cell proliferation to explain the antitumoral properties reported for these compounds. Supported by Junta de Castilla y León (6.000 €). 2005. IP Carlos Villalobos.

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