Daniela Leronni, PhD

  • Research Instructor

Daniela Leronni, PhD, has been a research instructor at the University of Pittsburgh Department of Neurological Surgery since January 2017.

She earned her BS/MS in biological sciences with a thesis in molecular biology at the University of Bari, Italy, in 2007. She completed her doctorate in genetics and molecular evolution at the University of Bari, in 2011.

Dr. Leronni’s early work as a PhD student and research assistant at the University of Bari from 2008 to 2011 focused on the functional characterization of genetics elements in the genome of model organisms with a low number of chromosomes, such as Drosophila Melanogaster (fruit fly) and Culex Quinquefasciatus (southern house mosquito). She studied the insulator activity of retrotransposons, genomic elements present in all organisms’ genome. The study of the genetics of regulatory elements was the basis for Dr. Leronni’s background in molecular biology and her interest in gene therapy.

In 2009, Dr. Leronni was offered a fellowship as a visiting research student in the Department of Surgery at Harvard University. Here she contributed to the finding that demonstrates that mitochondria host segregated cAMP cascades with distinct functional and kinetic signatures. In this way, she began to investigate biological mechanism at a cellular level and applied her knowledge in molecular biology to carry on research in cellular biology.

In 2012, Dr. Leronni joined the University of Pittsburgh via the Department of Microbiology and Molecular Genetics as a postdoctoral associate. Under the supervision of Joseph C. Glorioso III, PhD, she gained experience in the design and generation of gene therapy vectors that can be used to deliver multiple protective genes simultaneously to neurons, with the long-term goal of using these vectors as new approaches to neurological disease.

In 2015, Dr. Leronni was recruited by Robert Friedlander, MD, as postdoctoral associate to develop novel approaches for gene therapy for Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS) and to study the basic mechanism of these diseases. One of the main objectives of her research is the creation of gene therapy vectors for HD, including, vectors targeting melatonin synthesis, which plays a protective role in the brain. Additionally, Dr. Leronni leads a research project investigating mitochondrial dysfunction in neurodegenerative disease and mitochondria signal transduction.

Dr. Leronni's publications can be reviewed through the National Library of Medicine's publication database.

Specialized Areas of Interest

Molecular biology; neurodegenerative diseases; gene therapy; mitochondria.

Board Certifications

Biologo Professionista, Italy

Professional Organization Membership

American Association for the Advancement of Science
National Center for Faculty Development & Diversity

Education & Training

  • BS/MS, Biology/Molecular Genetics, Università degli Studi Aldo Moro, Bari, Italy, 2007
  • Research Scholar, Cell Signaling, Harvard Medical School, 2010
  • PhD, Genetics and Molecular Evolution, Università degli Studi Aldo Moro, Bari, Italy, 2011
  • Postdoctoral Fellowship, Molecular Genetics/Gene Therapy, University of Pittsburgh, 2014
  • Postdoctoral Fellowship, Neurodegenerative Diseases, University of Pittsburgh, 2016

Research Activities

In the past year, Dr. Leronni continued to investigate the functional meaning of the mitochondria localization of the Melatonin receptor 1 (MT1) and the receptor-mediated neuroprotective effect of melatonin. This project arises from Dr. Friedlander group’s groundbreaking discovery that MT1 is dually localized on the plasma membrane and the outer mitochondria membrane (OMM). The hypothesis of the project is that the dually localized MT1 receptors have two distinct functions and that the hormone melatonin acts as neuroprotector through its mitochondrially localized MT1 receptor. In the past year, Dr. Leronni generated molecular biology tools that allowed her to identify the post-translational modification required for the correct plasma membrane localization of the receptor, but not for its mitochondrial localization. In addition, she continues to collaborate with other researchers to study the mitochondrial signaling cascade triggered by melatonin and its receptors in brain of mice models.