Dmitry Lim

Graduated from the Moscow State University in Physiology com Laude, I obtained my PhD from the London University of London and the Naples Zoological Station in Naples, Italy, in Physiology and Cell Biology. My PhD project, led by Dr. Luigia Santella, was on the role of Ca2+-related second messengers IP3, NAADP and cADPr in fertilization of starfish oocytes. Dr. Santella and her skilful technician Dr. Giovanni Gragnagniello introduce me to the magic world of Ca2+ signaling and fluorescent microscopy, techniques, which became my core expertise throughout my carrier.

After PhD, I moved to the Lab of Prof. Ernesto Carafoli at the University of Padova and Venetian Institute of Molecular Medicine. Here I gained interest to neurosciecnce as well as the understanding of the complexity of neurodegenerative diseases. My project focused on decifering mitochondrial dysfunction in striatal neurons in Huntington's disease. During these years, Prof. Marisa Brini instilled me a love of molecular biology and viral gene delivery, powerful tools of manipulating with genes and proteins inside the cell.

In search of new opportunities, I moved to Novara, to the Lab of Prof. Armando Genazzani at the Università del Piemonte Orientale. Armando gave me unconditional support in a new adventure into astroglial pathophysiology and role of astrocytes in Alzheimer's disease. With his sage advises he guided me to scientific independence and leadership.

Supported by a grant from Cariplo Foundation, I consolidated my research in gliobiology demostrating a key role of astrocytic calcineurin in development of Alzheimer's disease. For this I generated and characterized mice with an astrocyte-specific inducible calcineurin deletion on the background of 3xTg-AD mouse model. We demonstrated that genetic deletion of a regulatory calcineurin B1 subunit (CNB1) from GFAP-expressing astrocytes fully prevents beta-amyloid and tau neruopathology, neuroinflammation and cognitive flexibility in 3xTg-AD mice.

Currently, we are working on understanding the mechanisms by which deleton of CNB1 prevents AD progression in order to identify target(s) for therapeutic intervention.

In course of the last decade, research on astrocytic calcium-calcineurin signaling brought me to an understanding that dysfunctions of different pathways and processes in Alzheimer's disease astrocytes, such as Ca2+ signaling, bioenergerics, oxidative stress, protein synthesis and degradation, and, ultimately, the prototypic homeostatic support to neurons and other cells in the CNS, may have a common denominator. Research of the last several years of the Lab suggests that this denominator is represented by ER-mitochondria contact sites (MERCS), platforms at which ER and mitochondria communicate to each other to coordinate many, if not all, cellular processes. Guided by this discovery, my current research interests are focused on understanding of mechanisms by which MERCS coordinate cellular functions and on identifying approaches of manipulating with MERCS in order to restore astrocytic homeostasis in Alzheimer's disease and other pathological conditions.