Prof. Dr. Mathias Jucker

Group Leader
Prof. Jucker is board director at the Hertie Institute for Clinical Brain Research

German Center for Neurodegenerative Diseases (DZNE)
Otfried-Müller-Straße 27
72076 Tübingen

mathias.jucker(at)dzne.de
+49 (0) 7071 / 29-86863
+49 (0) 7071 / 29-4521

Group members

Name Telefon Fax
Mehtap Bacioglu, PhD student +49 (0) 7071 29-81924 +49 (0) 7071 29-4521
Melanie Barth, PhD student +49 (0) 7071 29-81945 +49 (0) 7071 29-4521
Timo Eninger, PhD student +49 (0) 7071 29-81945 +49 (0) 7071 29-4521
Dr. Susanne Gräber-Sultan, Scientist
Lisa Häsler, Scientist +49 (0) 7071 29-86862 +49 (0) 7071 29-4521
Elke Kuder-Buletta, Study nurse +49 (0) 7071 29-87584 +49 (0) 7071 29-4521
Dr. Jonas Neher, Research Group Leader +49 (0) 7071 29-87596 +49 (0) 7071 29-4521
Oliver Preische, Physician +49 (0) 7071 29-85146 +49 (0) 7071 29-4521
Dr. Angelos Skodras, Research Group Leader +49 (0) 7071 29-87607 +49 (0) 7071 29-4521
Katleen Wild, Technical Assistant +49 (0) 7071 29-81951 +49 (0) 7071 29-452
Further group members (third party funding)
Jay Rasmussen, PhD student +49 (0) 7071 29-81945 +49 (0) 7071 29-4521
Juliane Schelle, PhD student +49 (0) 7071 29-81945 +49 (0) 7071 29-4521
Shot at the Hertie Institute for clinical Brain Research (HIH).
Shot at the Hertie Institute for clinical Brain Research (HIH).Click on the magnifying glass for a large image.

Selected publications

Neurofilament light chain in blood and CSF as marker of disease progression in mouse models and in neurodegenerative diseases.

Bacioglu M, Maia LF, Preische O, Schelle J, Apel A, Kaeser SA, Schweighauser M, Eninger T, Lambert M, Pilotto A, Shimshek D, Neumann U, Kahle PJ, Staufenbiel M, Neumann M, Maetzler W, Kuhle J, Jucker M; (2016)  Neuron 91: 56-66. 

Persistence of Aß seeds in APP-null mouse brain.

Ye L, Fritschi SK, Schelle J, Obermüller U, Degenhardt K, Kaeser SA, Eisele YS, Walker LC, Baumann F, Staufenbiel M, Jucker M (2015) . Nature Neuroscience 18: 1559- 1561.

Formaldehyde-fixed brain tissue from spontaneously ill α-synuclein transgenic mice induces fatal α-synucleinopathy in transgenic hosts.

Schweighauser M, Bacioglu M, Fritschi SK, Shimshek DR, Kahle PJ, Eisele YS, Jucker M (2015)  Acta Neuropathologica 129: 157-9.

Replacement of brain-resident myeloid cells does not alter cerebral amyloid-ß deposition in mouse models of Alzheimer´s disease.

Varvel NH, Grathwohl SA, Degenhardt K, Resch C, Bosch A, Jucker M, Neher JJ (2015) . Journal of Experimental Medicine 212: 1803-1809.

Increased CSF Aβ during the very early phase of cerebral Aβ deposition in mouse models.

Maia LF, Kaeser SA, Reichwald J, Lambert M, Obermüller U, Schelle J, Odentghal J, Martus P, Staufenbiel M, Jucker M (2015)  EMBO Mol Med 7: 895-903.

Highly potent soluble Aβ seeds in human Alzheimer brain but not cerebrospinal fluid.

Fritschi SK, Langer F, Kaeser SA, Maia L, Maetzler W, Keyvani K, Spitzer P, Wiltfang J, Staufenbiel M, Jucker M (2014) Brain 137: 2909-15.

Self-propagation of pathogenic protein aggregates in neurodegenerative diseases.

Jucker M, Walker LC (2013) Nature 501: 45-51.

Seeded strain-like transmission of β -amyloid morphotypes in APP transgenic mice.

Heilbronner G, Eisele YS, Langer F, Kaeser SA, Novotny R, Nagarathinam A, Aslund A, Hammarstrom P, Nilsson KPR, Jucker M (2013) EMBO reports 14: 1017-1022.

Changes in amyloid-b and Tau in the cerebrospinal fluid of transgenic mice overexpressing amyloid precursor protein.

Maia LF, Kaeser SA, Reichwald J, Hruscha M, Martus P, Staufenbiel M, Jucker M (2013) Science Translational Medicine 5: 194re2.

Microglia repopulation model reveals a robust homeostatic process for replacing CNS myeloid cells.

Varvel NH, Grathwohl SA, Baumann F, Liebig C, Bosch A, Brawek B, Thal DR, Charo IF, Heppner FL, Aguzzi A, Garaschuk O, Ransohoff RM, Jucker M (2012) Proc. Natl. Acad. Sci. USA 109: 18150-18155.

The amyloid state of proteins in human diseases.

Eisenberg D, Jucker M (2012) Cell 148: 1188-1203.

Soluble Aβ seeds are potent inducers of cerebral β-amyloid deposition.

Langer F, Eisele YS, Fritschi SK, Staufenbiel M, Walker LC, Jucker M (2011) Journal of Neuroscience 31: 14488-14495.

Peripherally applied Aß-containing inoculates induce cerebral ß-amyloidosis.

Eisele YS, Obermueller U, Heilbronner G, Baumann F, Kaeser SA, Wolburg H, Walker LC, Staufenbiel M, Heikenwalder M, Jucker M (2010) Science 330: 980-982.

Curriculum Vitae

Mathias Jucker, Ph.D., is Professor of Cellular Neurology at the Hertie Institute for Clinical Brain Research at the University of Tübingen and the German Center for Neurodegenerative Diseases (DZNE) in Tübingen, Germany. He earned his Ph.D. at the Swiss Federal Institute of Technology in  Zürich. His main areas of research are the cellular and molecular mechanisms responsible for brain aging and Alzheimer’s disease. He has made groundbreaking discoveries in the fundamental mechanisms underlying neurodegenerative diseases, such as the role of self-propagating pathogenic protein aggregates in Alzheimer’s disease and other disorders of the aging brain. Noteworthy are his efforts to translate fundamental research into clinical studies and his commitment to the Dominantly Inherited Alzheimer Network (DIAN). He is the speaker of the Graduate School of Cellular and Molecular Neuroscience in Tübingen. For his research he has received several honors and prizes, most recently the Science Prize for Dementia Research of the Academy of Sciences, Hamburg, Germany (2013), and the MetLife Award for Medical Research of the MetLife Foundation, New York (2014).


Areas of investigation/research focus

 

The focus of our research is on the cellular and molecular mechanisms of brain aging and age-related neurodegenerative diseases, with a special emphasis on the pathogenesis of Alzheimer´s disease and other cerebral amyloidoses.

We do primarily basic research with a focus on preclinical investigations of disease mechanisms. To foster the translation of our research to clinical applications, we coordinate the international Dominantly Inherited Alzheimer Network (DIAN) study in Germany, which aims to understand the rare genetic forms of Alzheimer's disease by longitudinal analysis of gene mutation carriers and non-mutation carrier siblings. Understanding this type of Alzheimer's disease is expected to provide important clues to the development of the more common sporadic form of Alzheimer´s disease.

Our department is part of the DZNE and the Hertie Institute of Clinical Brain Research at the University of Tübingen.

A more detailed descripition of the research can be found on the cooperation partner's homepage here.