Phenotypes are the result of the combination of genetic and environmental factors, which are expressed via multiple molecular pathways throughout our lives. Aberrant alteration of those pathways elicits pathological phenotypes in cells, tissues, and organs that characterize specific diseases. Our group uses computational and experimental approaches to understand and correct the pathological phenotype using drugs applied individually and in combination. Our aim is to identify new target and finally lead molecules that can be developed in drug.

Our focus area is to investigate how the crosstalk between CNS and immune system contribute to generate disease phenotypes in the main neurodegenerative diseases. In particular we are focusing our interest in Alzheimer’s disease and Fronto Temporal Dementia.

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Phenotypic alterations are the causes of disease, whether this is a cancer cell undergoing uncontrolled cell division or the complex defects seen in the brain of a patient with Alzheimer’s disease. Screening for agents that alter a phenotype is an effective route to find new therapies and to understand the molecular events involved in disease.

To achieve this aim our group make use of large-scale experimental approaches and combining quantitative “omics” data with high-content screens and computational biology we aim to better understand the underlying mechanisms of may provide strategies for the prevention and the treatment of pathological conditions.

To achieve our goals we use cell biology, stem cells, tissue engineering, high-content screening, high-content analysis, laboratory automation and computational biology.


Wera Roth, David Hecker, Eugenio Fava. Systems biology approaches to the study of biological networks underlying Alzheimer's disease: Role of miRNAs 2015.
Gilleron J, Querbes W, Zeigerer A, Borodovsky A, Marsico G, Schubert U, Manygoats K, Seifert S, Andree C, Stöter M, Epstein-Barash H, Zhang L, Koteliansky V, Fitzgerald K, Fava E, Bickle M, Kalaidzidis Y, Akinc A, Maier M, Zerial M. Image-based analysis of lipid nanoparticle-mediated siRNA delivery, intracellular trafficking and endosomal escape. Nat Biotechnol. 2013 Jul 01; 31:638-46. doi: 10.1038/nbt.2612
Collinet C, Stöter M, Bradshaw CR, Samusik N, Rink JC, Kenski D, Habermann B, Buchholz F, Henschel R, Mueller MS, Nagel WE, Fava E, Kalaidzidis Y, Zerial M. Systems survey of endocytosis by multiparametric image analysis. Nature. 2010 Mar 11; 464:243-9. doi: 10.1038/nature08779
Bramsen JB, Laursen MB, Nielsen AF, Hansen TB, Bus C, Langkjaer N, Babu BR, Højland T, Abramov M, Van Aerschot A, Odadzic D, Smicius R, Haas J, Andree C, Barman J, Wenska M, Srivastava P, Zhou C, Honcharenko D, Hess S, Müller E, Bobkov GV, Mikhailov SN, Fava E, Meyer TF, Chattopadhyaya J, Zerial M, Engels JW, Herdewijn P, Wengel J, Kjems J. A large-scale chemical modification screen identifies design rules to generate siRNAs with high activity, high stability and low toxicity. Nucleic Acids Res. 2009 May 01; 37:2867-81. doi: 10.1093/nar/gkp106
Pelkmans L, Fava E, Grabner H, Hannus M, Habermann B, Krausz E, Zerial M. Genome-wide analysis of human kinases in clathrin- and caveolae/raft-mediated endocytosis. Nature. 2005 Jul 07; 436:78-86.

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