I am a postdoctoral scholar in the laboratory of Dr. Bacskai at Massachusetts General Hospital (MGH) and Harvard Medical School, Boston. My long-term research goal is to understand the mechanisms that lead to the pathophysiology and neurodegeneration underlying neurodegenerative disorders, most particularly Alzheimer’s disease (AD). Previously, my PhD work focused on the role of calcium (Ca2+) signaling in aging and AD. I trained as PhD student at the Chemoprevention and Neuroprotection group, at the Institute of Molecular Biology and Genetics (IBGM), funded by the Spanish Research Council and the University of Valladolid, headed by Dr. Villalobos and Dr. Nunez. During my PhD, I trained in intracellular Ca2+ physiology and its involvement in pathology, specifically in aging and in neurodegenerative disorders such as ischemia and AD. I implemented an in vitro model of aging and AD that allowed me to study the remodeling of Ca2+ homeostasis as well as subcellular (organellar) Ca2+ in these pathologies. To carry out this research, I specialized in different techniques, including fluorescence and bioluminescence imaging techniques, and most specifically in Ca2+ imaging. My current research focuses on the mitochondrial dysfunction in AD, particularly in mitochondrial Ca2+ dysregulation and associated oxidative stress and neuronal cell death that accounts in AD. Specifically, I use in vivo multi-photon microscopy to study mitochondrial alterations in models of cerebral amyloidosis and tau pathology. In vivo multi-photon microscopy is an extremely powerful tool to study pathophysiological processes in real-time in the living mouse.
For this work I was awarded a Tosteson & Fund for Medical Discovery (FMD) Postdoctoral Fellowship Award from the Massachusetts General Hospital. I also recently received a BrightFocus Foundation Fellowship to continue with my research and study the role of mitochondria in astrocytes and their potential dysregulation in AD. In terms of future research directions, I am interested in understanding how amyloid beta (Aβ) and tau pathology affect organelles, more specifically in the ER dysfunction and the disruption of the ER-mitochondria coupling. These alterations may reduce the production of ATP, affect the long-term storage memory and cause cell death. If they are a cause or a consequence of the pathology is still unknown. I was very fortunate to join by early 2016 the group of Dr. Bacskai. Dr. Bacskai is an internationally renowned expert in the field of intravital imaging. He pioneered the use of in vivo multi-photon imaging in stablished models of AD. He offers great support to me, an early investigator, and provides excellent guidance and scientific freedom to take the next steps towards becoming an independent researcher. The scientific environment in which I work – Massachusetts General Hospital and Harvard Medical School – allows me to use state of the art es and to interact with world-renowned experts in the field of both neurodegenerative diseases and optics/imaging. During my years as a pre-doctoral and more recently post-doctoral researcher, I have had the opportunity of mentoring of several students and I am continuing to extend my role as a supervisor. Receiving the prestigious New Vision Investigator Award will provide me the necessary time and money to complete my experimental training in multi-photon microscopy, and in the field of Alzheimer’s disease, as well as add a new set of skills, and will undoubtedly be instrumental for the transition into an independent researcher