© estudio pobrelavaca 2006
       
   

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.

 
       
   

2001 - 2004

Mechanisms involved in neuronal cell damage: subcellular Ca2+ and specific gene espression.
Mitochondrial Ca2+ and expression of several genes as Bcl2 is involved in neurons cell death. However, monitoring of these parameters in individual neurons is difficult. Here we propose to measure changes in mitochondrial Ca2+ and expression of specific genes at the single cell level by bioluminescence imaging of primary neurons expressing either targeted aequorins or luciferase under control of specific gene promoters.
Supported by Junta de Castilla y León (11.213 €). 2002-2004. IP Lucía Núñez.