BIO
Dr. Edward Málaga-Trillo was born in Lima, Perú, completed his undergraduate studies in Biology at Universidad Peruana Cayetano Heredia (UPCH) and carried out his Ph.D. in Microbiology and Immunology at the University of Miami School of Medicine and the Max-Planck-Institut für Biologie in Tübingen, Germany. After postdoctoral trainings in Evolutionary Genomics and Developmental Neurobiology at the University of Konstanz, Germany, he was appointed Wissenschaftlicher Assistent (Assistant Professor) there and, upon completing the German Habilitation, Privatdozent (Adj. Associate Professor) in Developmental Neurobiology. Throughout his career, he acquired specialized training in fish genetic manipulations (Stirling, Scotland), Molecular Evolution (Hayama, Japan), Evolutionary Genomics (Eugene, USA) and Developmental Genetics of Zebrafish (Woods Hole, USA). His published work focuses on the cellular and molecular basis of neuronal degeneration and regeneration. Dr. Málaga-Trillo’s uses zebrafish as a model organism to study molecular mechanisms of neurodegeneration. In 2015 he returned as Full Professor to UPCH, where he set up the first Peruvian zebrafish laboratory at the Developmental Neurobiology Research Unit. Since 2018 he is President of the Latin American Zebrafish Network (LAZEN).

RESEARCH INTERESTS
Neurodegenerative conditions like Alzheimer’s, Parkinson’s and prion disease result from the misfolding and aggregation of key neuronal proteins. In fact, the striking loss of cognitive and motor abilities in these age-related illnesses is frequently linked to the appearance of abnormal protein deposits in neurons. However, the presence of plaques and tangles in elderly brains is not a precondition for neurodegeneration. Rather, neuronal damage is triggered by small precursors of these rogue proteins decades before brain deposits and clinical symptoms become evident.

Our research has two continuing goals:

-understanding the cellular and molecular mechanisms by which misfolded protein oligomers induce early neurotoxicity in vivo
-transforming this information into novel drug screening methodologies to identify anti-neurodegeneration compounds

To pursue these goals, we employ cell biological, biochemical and behavioral approaches in genetically and pharmacologically manipulated zebrafish embryos. These small vertebrates offer key experimental advantages, such as their external development and optical clarity, which allow for high resolution imaging of physiological processes in neurons.

Of special interest to our lab is the involvement of the cellular prion protein (PrPC) as a common receptor for various neurotoxic species in the brain, including amyloid β (aβ), α-synuclein and its own misfolded isoform, PrPSc. This intriguing role of PrPC as a broad transducer of neurotoxicity relies on its physiological ability to elicit complex intracellular signals. Therefore, many of our efforts are aimed at analyzing how PrP modulates molecular pathways and cellular events in health and disease.

Currently, our projects center around the following topics:

-The complex roles of PrPC- and SFK-associated pathways during early morphogenesis and neural development, their genetic redundancy and compensatory mechanisms, maternal and zygotic gene functions.
-Neurotoxic pathways induced by amyloids in vivo and their connection to the PrPC/SFK-mediated control of neuroreceptor and adhesion molecule activity.
-Spatiotemporal dynamics of amyloid aggregation in the nervous system, their cellular uptake and processing.
-Development of embryo-based neurotoxicity reporter assays to screen for anti-neurodegeneration drugs.