Carlos Alós-Ferrer named NOMIS Professor for Decision and Neuroeconomic Theory at the University of Zurich

Carlos Alós-Ferrer has been appointed NOMIS Professor for Decision and Neuroeconomic Theory at the University of Zurich (UZH) in Switzerland. He is an economist who, prior to joining UZH, was professor of microeconomics at the University of Cologne, Germany, and the speaker of the interdisciplinary research unit “Psychoeconomics,” funded by the German Research Foundation (DFG). He studied mathematics at the University of Valencia, Spain, and received his PhD in Economics at the University of Alicante, Spain, in 1998.

Alós-Ferrer has conducted research on game theory and mathematical economics, and has a strong interest in neuroeconomics (also known as psychoeconomics), the interdisciplinary field that combines psychology, economics and neuroscience to study human decision making.

The goal of neuroeconomics is to provide a foundation for the study of underlying neural processes of decision-making within today’s economic environment. Essential to the further progress of this field is the construction of empirically informed, testable models that connect the level of neural and mental processes underlying decision-making with the descriptive models of choice that characterize modern economics. Through this professorship, Alós-Ferrer will draw on the collaborative, interdisciplinary expertise at UZH to develop viable models with the potential to have a significant impact on the field of neuroeconomics.

The NOMIS Professorship for Decision and Neuroeconomic Theory is a result of a long-term partnership among the Department of Economics at UZH, the Excellence Foundation and the NOMIS Foundation.

Jacob Corn named Professor of Genome Biology at ETH Zurich

Jacob Corn has been appointed Professor of Genome Biology at ETH Zurich. Corn is the founding scientific director of the Innovative Genomics Institute and adjunct assistant professor at the University of California, Berkeley. His research aims to bring about the end of genetic disease through the development and application of next-generation genome editing technologies — improving human health through the fundamental understanding of disease mechanisms.

Corn’s experience extends to therapeutic areas that include infectious disease, neurobiology and oncology, and his work has redefined our understanding of DNA replication. He computationally designed protein inhibitors from scratch and discovered biological mechanisms for challenging therapeutic targets.

The key objective of the ETH professorship, which is funded by NOMIS in cooperation with the Lotte und Adolf Hotz-Sprenger Stiftung, is to study the functional elements encoded in complex genomes through comparative analysis, seeking to deepen our understanding of how the genetic variation in the human population is related to disease susceptibility.

Corn is exploring processes that detect and repair damage to DNA, using these findings to repair, switch on or off, or replace genes in the genome at a defined position. This knowledge is important for both therapeutic use as well as basic and applied research.

Salk Institute: “Alzheimer’s drug turns back clock in powerhouse of cell”

Salk researchers have identified the molecular target of J147. The experimental drug is something of a modern elixir of life; it’s been shown to treat Alzheimer’s disease and reverse aging in mice and is almost ready for clinical trials in humans. Now, Salk scientists have solved the puzzle of what, exactly, J147 does. In a paper published January 7, 2018, in the journal Aging Cell, they report that the drug binds to a protein found in mitochondria, the energy-generating powerhouses of cells. In turn, they showed, it makes aging cells, mice and flies appear more youthful.

“This really glues together everything we know about J147 in terms of the link between aging and Alzheimer’s,” says Dave Schubert, head of Salk’s Cellular Neurobiology Laboratory and the senior author on the new paper. “Finding the target of J147 was also absolutely critical in terms of moving forward with clinical trials.”

Schubert’s group developed J147 in 2011, after screening for compounds from plants with an ability to reverse the cellular and molecular signs of aging in the brain. J147 is a modified version of a molecule (curcumin) found in the curry spice turmeric. In the years since, the researchers have shown that the compound reverses memory deficits, potentiates the production of new brain cells, and slows or reverses Alzheimer’s progression in mice. However, they didn’t know how J147 worked at the molecular level.

In the new work, led by Schubert and Salk Research Associate Josh Goldberg, the team used several approaches to home in on what J147 is doing. They identified the molecular target of J147 as a mitochondrial protein called ATP synthase that helps generate ATP—the cell’s energy currency—within mitochondria. They showed that by manipulating its activity, they could protect neuronal cells from multiple toxicities associated with the aging brain. Moreover, ATP synthase has already been shown to control aging in C. elegans worms and flies.

The Salk Institute has been a NOMIS partner since 2008.

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Aging Cell: “The mitochondrial ATP synthase is a shared drug target for aging and dementia”

Scientists at the Salk Institute have published the results of a study in the journal Aging Cell, showing the novel molecular link between aging and dementia through the identification of the molecular target for the Alzheimer’s disease drug J147.

Led by Dave Schubert, head of Salk’s Cellular Neurobiology Laboratory, and Salk Research Associate Josh Goldberg, the team identified the molecular target of J147 as a mitochondrial protein called ATP synthase that helps generate ATP—the cell’s energy currency—within mitochondria. They showed that by manipulating its activity, they could protect neuronal cells from multiple toxicities associated with the aging brain. Moreover, ATP synthase has already been shown to control aging in C. elegans worms and flies. Now, J147 is nearing clinical trials to treat Alzheimer’s disease.

The Salk Institute has been a NOMIS partner since 2008.

Salk Institute: Immune receptors amplify “invader” signals by turning into mini-machines

Researchers at the Salk Institute in La Jolla, California, have discovered how immune receptors use a protein to amplify “invader” signals and attack a biological intruder. The T cell receptor that detects the intruder activates and releases copy after copy of a protein called ZAP70, becoming a mini-machine. This discovery sheds light on how T cells identify and react to pathogens — something researchers have for decades struggled to explain — and could help scientists develop better treatments for immune-based cancer and autoimmune diseases.

The research is supported in part by the NOMIS Foundation, and the finding was published on Nov. 21, 2016, in Nature Immunology. More details can be found in the Nov. 21 release by the Salk Institute.

The Salk Institute has been a NOMIS partner since 2008.

NOMIS researcher links heart disease, leukemia and aging disorders to dysfunction in nucleus

Salk Institute scientists in La Jolla, California have published in the Nov. 2 issue of Genes & Development a study demonstrating that the nuclear membrane acts not only as a driver of gene expression, but also disease. NOMIS board member and professor of molecular and cell biology at the Salk Institute Martin Hetzer is leading the team, who discovered that two proteins in the nuclear envelope, along with the membrane-spanning complexes they form, interact with parts of the genome to trigger key gene expression.

These proteins regulate the expression of super-enhancer-driven genes—i.e., those that help determine cell identity—and abnormal gene expression occurs when either of the proteins are suppressed. Experiments with human bone cancer and lung cancer cell lines confirmed that altering the proteins Nup153 or Nup93 result in faulty gene expression.

In the release published by Salk, Hetzer says, “People have thought the nuclear membrane is just a protective barrier, which is maybe the reason why it evolved in the first place. But there are many more regulatory levels that we don’t understand. And it’s such an important area because so far, every membrane protein that has been studied and found to be mutated or mis-localized, seems to cause a human disease.”

By better understanding this process, greater insight into diseases such as heart disease, leukemia and aging disorders, which are thought to be related to dysfunctional nuclear membrane components, can be gained.

The Salk Institute has been a NOMIS partner since 2008.