Aging is a crucial risk factor in a constellation of human diseases, including cancer and neurodegenerative diseases. Along with other risk factors such as environmental exposures, diet, behavior, and heredity, these risks can be understood through their impact on the epigenetic landscape in ways that ultimately lead to the burden of disease. Among these risks, aging had been regarded as fixed, but current thinking holds that aging is plastic and its pace can be slowed or even reversed. Dr.
Autophagy is an essential catabolic cellular process that assures the maintenance of the cellular energetic balance as wells as an efficient removal of any intracellular damaged structure. In this talk, Dr. Cuervo will focus on selective forms of autophagy, and describe her lab’s recent advances on the identification of new molecular effectors and regulators for these pathways, the physiological role, and their changes in aging and age-related metabolic disorders and neurodegenerative diseases such as Parkinson, Alzheimer and Huntington disease.
Douglas C. Wallace, Ph.D. The Children’s Hospital of Philadelphia and Perelman School of Medicine, University of Pennsylvania
For half a millennium Western medicine has focused on anatomy and for the past century on nuclear DNA (nDNA), Mendelian, genetics. While these concepts have permitted many biomedical advances, they have proven insufficient for understanding the common “complex” diseases. Life requires energy, 90 percent of which comes from the mitochondrion. The mitochondrial genome consists of thousands of copies of the maternally inherited mitochondrial DNA (mtDNA) plus 1,000–2,000 nDNA genes.
Raju S. Kucherlapati, Ph.D. Harvard Medical School
The understanding of the genetics and genomics of cancer is changing very rapidly. The ability to use next-generation sequencing technologies to dissect the genomes of individual cancer patients is helping to drive this increase in knowledge. In his lecture, Dr. Kucherlapati will describe some of the recent advances and how that knowledge is shedding light on the biology of cancer and helping us develop novel therapeutic approaches.
Proper functioning of the nervous system requires that neurons assemble their stereotypic wiring patterns during development, as well as maintain these connectivity patterns throughout life. In disease, however, surviving neurons rewire inappropriately as the circuits disassemble. Dr. Wong’s laboratory is interested in elucidating the cellular interactions that shape developing circuits in the retina, and in understanding the capacity by which regenerating circuits can recapture their original synaptic arrangements during repair. During the lecture, Dr.
Peter Palese, Ph.D. Mount Sinai School of Medicine
Because influenza viruses are constantly changing, it’s difficult to develop effective vaccines against them. Two molecules on the surface of the virus control its infectivity: hemagglutinin and neuraminidase. Current influenza virus vaccines predominantly elicit a protective immune response to the immunodominant but variable head of the hemagglutinin. This approach is effective, especially when the vaccine strain closely matches the circulating virus.
Ulrike A. Heberlein Howard Hughes Medical Institute – Janelia Farm Research Campus
Alcohol is one of the most widely used and abused drugs in the world with devastating medical and social consequences. The estimated prevalence of Alcohol Use Disorders is 8.5 percent in the United States, thus affecting more than 17 million Americans. The difficulty and cost of human studies have led to the development of animal models to investigate the genetic, molecular, and neural mechanisms underlying both the short- and long-term effects of ethanol. Rodent models have been most widely used and have provided important insights into these mechanisms.
Research over the past two decades has led to the fundamental understanding that initiation of immune responses to infectious microorganisms relies on pathogen recognition by innate microbial sensors, collectively known as pattern recognition receptors (PRRs). PRRs fall into several families, each of which recognizes distinct pathogen-associated molecular patterns (PAMPs). Stimulating PRRs results in transcriptional activation of genes involved in innate defense as well as those that activate antigen-presenting cells for successful priming of “adaptive” T- and B-cell responses.
C. Ronald Kahn, M.D. Joslin Diabetes Center, Harvard Medical School
Both type 2 diabetes and obesity are the result of complex interactions between genes and environment and between adipose tissue (fat) and other tissues of the body. For example, fat releases adipokines that influence insulin action in other tissues; there are increasingly complex effects of the brain and adipose tissue on the control of metabolism.
Our understanding of the reaction mechanisms of membrane-embedded transport proteins or enzymes is insufficient. Dr. Kaspar Locher’s research group investigates two distinct types of membrane proteins, ATP-driven transporters and oligosaccaryltransferase (OST). In the past decade, his lab’s structural studies have defined the transmembrane folds of type 1 and type 2 ABC importers, ABC exporters, and of the catalytic subunit of OST.
This page was last updated on Tuesday, August 10, 2021
