Federica del Monte is a clinician-scientist, Associate Professor in Medicine in the Department of Medicine, Division of Cardiology at the Medical University of South Carolina, Director of the Christie’s Heart & Brain Program. This will represent the first program to study the mechanisms linking those two diseases either as a systemic or metastatic condition and to care for patients with Heart Failure and Alzheimer’s in the hospital. She is also Associate Professor of Medicine at the Massachusetts General Hospital, Harvard Medical School in Boston where she developed her USA career over 20 years. She is an MD and Cardiology graduate from the University of Rome (Italy) and PhD graduate from the Imperial College of Science and Technology in London (UK).
Dr. del Monte’s lab focuses on basic cardiac muscle pathophysiology and translational research to understand the pathogenesis of cardiomyopathies and heart failure (HF) as an Alzheimer’s disease and for the discovery of novel therapies. The lab utilizes an interdisciplinary approach in-vitro and in-vivo physiology, molecular biology and imaging as well as biophysical and structural-chemistry approaches.
The early work from Dr. del Monte’s lab focused on Ca2+ homeostasis in the failing heart and gene therapy. For those studies, Dr. del Monte is a recognized leader in cardiomyocytes physiology and Ca2+ handling in animal models and human hearts. Dr. del Monte’s research has evolved towards cutting edge and
innovative unexplored territories linking Alzheimer’s Disease and heart failure. The latest discoveries are recognized as a major breakthrough that opened a new era for the understanding of the pathogenesis of HF.Dr. del Monte discovered, in dilated cardiomyopathy (iDCM), plaque and tangles-like protein aggregates similar to the pathological defects in Alzheimer Disease (AD). Since this first discovery the lab determined that Alzheimers Disease and cardiomyopathy share the same pathogenic defect changing the paradigm of the pathogenesis of iDCM. The lab characterized the cell response to misfolded proteins; identified genetic variants in common between iDCM and AD; purified and chemical characterized the composition of amyloid fibrils of cardiac plaques identifying an actin-polymerizing protein-Cofilin-2 to be comprised within the aggregates and characterized its role on cardiac function; identified how misfolded proteins exert their toxic effect and developed the new concept of metastatic transmissibility of pre-amyloid oligomers. In addition to identifying Alzheimer’s like plaques and tangles in the heart of patients with cardiomyopathy the lab determined that the heart of patients with primary diagnosis of Alzheimer’s contains Ab deposits and present diastolic dysfunction. Given the commonality of the structure/function of misfolded proteins, the results obtained on cardiomyocytes can be translated to any cell, and studying the heart can provide insights for the detection of onset and progression of brain disorders using the heart as a window to the brain and offering a common therapeutic target for diseases affecting millions of people.