Christian Haass, professor at Ludwig-Maximilians-University Munich and speaker of the DZNE site Munich, has received the Wissenschaftspreis 2022 (science award) endowed with 150,000 euros from the Weinheim-based Hector Stiftung II. With this award, the foundation honors the Munich biochemist’s groundbreaking research into the molecular mechanisms of Alzheimer's disease: Haass found that, in Alzheimer’s patients, the protein amyloid beta-peptide increasingly deposits in the brain in a toxic form that damages the neurons. The award was presented on Friday evening (January 27) in Heidelberg.
Award for cutting-edge research
The H. W. & J. Hector Stiftung was established in 1995 by Josephine and Dr. h. c. Hans-Werner Hector in Weinheim an der Bergstrasse. In 2008, the "Hector Stiftung II" was established as a supplement. Since 2009, the Hector Foundation II has awarded the annual Hector Wissenschaftspreis in the amount of 150,000 euros. This award honors professors at German universities and research institutions for their outstanding research achievements and special commitment to teaching and promoting young scientists.
This year, the Hector Stiftung II awarded the Hector Wissenschaftspreis to Prof. Dr. Dr. h.c. Christian Haass and the mathematician Prof. Dr. Anna Wienhard from the Max Planck Institute for Mathematics in the Sciences in Leipzig. The awards are endowed with 150,000 euros each. With this award, Haass and Wienhard - along with 27 other outstanding scientists - were admitted to the circle of "Hector Fellows" and will enrich interdisciplinary cooperation in the future as members of the "Hector Fellow Academy". The central concern of this young academy of science is to promote interdisciplinary exchange between its members, who work together across the limits of individual research institutions and across different disciplines.
Background information on the laureate
Christian Haass, born 1960 in Mannheim, Germany, studied biology in Heidelberg. He then did research at Harvard Medical School in the USA, where he eventually became assistant professor of neurology. This was followed by a professorship at the Central Institute of Mental Health, Mannheim (University of Heidelberg). In 1999 he was appointed Professor of Biochemistry at the Ludwig-Maximilians-University (LMU) Munich and head of the Department of Metabolic Biochemistry. Since 2009, Haass has also been site speaker for the DZNE Munich.
At the beginning of the 1990s Haass started working on a small protein called “amyloid beta-peptide”. This molecule aggregates in the brains of people with Alzheimer’s and forms deposits (called “plaques”) in the tissue between the neurons. These deposits lead to inflammatory processes. Eventually, tau fibrils form in the neurons, impairing their function and contributing to their cell death. The result of the massive death of nerves in the brain are the symptoms of Alzheimer's disease: memory and orientation disorders, speech disorders, impaired thinking and judgment, and personality changes. From a pathobiological perspective, Alzheimer's disease begins decades before the first memory deficits emerge, which means that the disease develops in the brain long before the first symptoms occur.
Contrary to what was thought at the time, Haass was able to prove that amyloid is not necessarily a component of pathological processes, but also occurs in the healthy brain. Today, it is therefore assumed that the production or degradation of this protein is disturbed in Alzheimer’s disease. In fact, Haass later discovered how genetic mutations associated with rare and early forms of Alzheimer’s cause overproduction of amyloid. As a result, this protein accumulates in the brain and the characteristic plaques develop. Haass’ research provided important insights into how amyloid is produced from a larger molecule (amyloid precursor protein) under the action of certain enzymes (secretases). His work and that of other scientists ultimately led to the formulation of the “amyloid cascade hypothesis”. According to this, amyloid plays an important role not only in the hereditary form of Alzheimer’s disease, by initiating a chain of events that ultimately leads to the death of brain cells. This also applies to the much more common, so-called sporadic variant of Alzheimer’s disease.
Christian Haass thus paved the way for therapeutic approaches aimed at preventing the formation of amyloid aggregates or promoting their degradation – and for new approaches to the early detection of Alzheimer's. In recent years, Haass extended his research to other aspects of Alzheimer’s disease and investigated the role of the immune cells of the brain: the “microglia”. Haass found that the so-called TREM2 protein triggers microglia to remove deposits of amyloid, particularly in the early stages of disease. Levels of TREM2 rise in the spinal fluid when microglia are activated. Accordingly, TREM2 could serve as a biomarker and contribute to the early detection of Alzheimer’s before symptoms manifest. Currently, Christian Haass is looking for approaches to specifically activate the microglia via an antibody in a way that the removal of plaques by the immune cells is stimulated.
Christian Haass has already received several awards for his research – including the Leibniz Prize of the Deutsche Forschungsgemeinschaft (German Research Foundation, DFG, the Brain Prize – the world's most prestigious award for brain research – and the Piepenbrock DZNE Prize. Christian Haass is also a member of the National Academy of Sciences Leopoldina and the Bavarian Academy of Sciences and Humanities, and holds an honorary doctorate from the University of Zurich.)