CENTRO DE BIOLOGÍA MOLECULAR SEVERO OCHOACaptura de pantalla 2022 09 14 a las 10.27.10    

Pathogenic mechanisms of Alzheimer’s disease

Research summary:

To identify genes and mechanisms involved in the neurodegeneration characteristic of Alzheimer's disease (AD), we developed cell models that reflect different aspects of the pathogenesis of the disease. These models allow us to identify new genes/functions associated with AD, which could be therapeutic targets for the disease. To do this, we analyze differential gene expression in the models and develop genetic association studies and biomarkers in clinical samples. In recent years, we have focused on models of herpes simplex virus 1 (HSV-1) infection that present characteristic markers of AD, including alterations in the trafficking, metabolism and proteolysis of the amyloid precursor protein (APP), as well as in the phosphorylation of the tau protein.

The study of the lysosome autophagy pathway in these models indicates that HSV-1, especially in the presence of oxidative stress, profoundly affects the final stages of the pathway, causing an increase in lysosomal content accompanied by a significant reduction in the activity of different cathepsins and in the degradation of lysosomal substrates. The evidence that another alpha-herpesvirus with neurotropic properties, HSV-2, induces the same neurodegeneration markers as HSV 1, supports the possible involvement of various infectious agents like as herpesviruses in AD-associated neurodegeneration.

The results of the functional and genetic/biomarker association studies developed so far support the hypothesis that lysosomal function failure could constitute a relevant mechanism in HSV-1-induced neurodegeneration and, in general, in AD type neurodegeneration, so our group is focused on the study of this functional pathway.  Currently, we are developing more complex cell models, based on human NPCs, to validate our previous findings in a more physiological environment and delve deeper into the mechanisms involved.

In addition, we participate in several collaborative projects. The most numerous are those aimed to study the genetic architecture of AD, within the framework of the Spanish Consortium for Dementia Genetics (DEGESCO) and the international consortia EADB and IGAP, which continue to reveal new factors and relevant functions in the pathogenesis of this disease.


LUHMES neurons on day 7 of differentiation labeled with MAP2 (red) and B-III tubulin (green) specific antibodies. DAPI-stained nuclei are also shown.


* For external calls please dial 34 91196 followed by the extension number
Last nameNameLaboratoryExt.*e-mailProfessional category
Aldudo SotoJesús4104674jaldudo(at)cbm.csic.esContratado Doctor CIBER
Beamonte PalomeroInés4104674Estudiante TFG
Bullido Gómez-HerasMª Jesús410/114.24567/ 4674mjbullido(at)cbm.csic.esProfesor Titular Universidad, GA
Martín RicoMaría4104674maria.martin(at)cbm.csic.esTitulado Sup.Inv.y Laboratorio
Recuero VicenteMaría4104674mrecuero(at)cbm.csic.esContratado Doctor CIBER
Romero SolaresAlba4104467Estudiante TFM
Salgado FuentesBlanca4104674bsalgado(at)cbm.csic.esContrato Predoctoral

Relevant publications:


  • Fundación Madrid+D. Premio a las mejores patentes; accésit. (2011)
  • Sociedad Madrileña de Neurología. Premio Ramón y Cajal de Investigación básica (2011)

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