Our scientific activity has been focused at studying pathophysiological mechanisms of neurodegenerative diseases, mainly Alzheimer’s disease and associated dementias, identifying new therapeutic targets, risk factors and biomarkers.
1. Preclinical studies on new risk factors, biomarkers of disease, mechanisms and new therapeutic strategies in Alzheimer’s disease and other neurodegenerative disorders.
a) Research on risk factors that highlight the relationship between metabolic disorders and neurodegenerative diseases, including Alzheimer’s, through mechanisms and inflammatory responses at central and peripheral level.
b) Preclinical research searching for new therapeutic targets and design of potential drugs using cellular and animal experimental models of Alzheimer’s disease and other degenerative dementias. Particularly we analysed the therapeutic efficiency of GDNF in Parkinson’s disease animal model. The intranasal administration of this compound allowed it to go through the BBB and avoided its quick degradation.
c) Studies on molecular pathology in neurodegenerative disorders analysing new pathophysiological mechanisms, in particular, mitochondrial alterations, as mitochondrial disfunction plays an important role in neurodegeneration. On this regard, we also studied alterations on mitochondrial dynamics and bioenergetics. Our results found proteinopathies resulting in cellular alterations including dementias.
2. Epidemiological research on neurodegenerative diseases, particularly risk factors.
a) Epidemiological analysis NEDICES-I cohort.
b) Implementation of NEDICES-II cohort: harvesting, processing and biobank storage of ~2000 subject samples recruited in Primary Care. Classification and verification of cases with neurodegenerative pathology.
3. Clinical research in dementia.
a) Collaboration searching for genetic risk factors, and participation in genetic consortia (DEGESCO).
b) Determination of clinical utility of molecular and imaging biomarkers recently introduced: new useful biomarkers for early detection of disease. In collaboration with other CIBERNED groups (M. Calero, A. Rábano and JL. Cantero), we have proposed salivary lactoferrin levels as early AD biomarker as it is reduced with the disease progression.
