Bayer, Thomas A., Prof. Dr.

Professor of Molecular Psychiatry

  • 1984-1989 Diploma in biology, University of Stuttgart and Whitney Lab Florida
  • 1989-1993 PhD at the University of Cologne (PhD Thyssen Graduate School)
  • 1993 Postdoctoral Research Fellow, University of Cologne, Cologne
  • 1993-1997 Postdoctoral Research Fellow, Institute of Neuropathology, University of Bonn Medical Center, Bonn
  • 1997-2002 Lab leader, Department of Psychiatry, University of Bonn Medical Center, Bonn
  • 2002-2007 Head of Neurobiology Lab, University of Saarland Medical Center, Homburg
  • 2004 Appointment to apl Professor at the University Medical Center Saarland
  • 2007-present University Professor in “Molecular Psychiatry” at the University of Göttingen, University Medical Center Göttingen
  • 2006-2011 Coordinator of the European Commission funded International Alzheimer PhD School «Neurodegeneration in Alzheimer’s disease – mechanism, consequence and therapy»

Major Research Interests

pathogenesis of Alzheimer’s disease, neuronal cell death mechanisms, preclinical proof-of-concept studies; characterization and development of mouse models for Alzheimer’s disease (neuropathology, anatomy, biochemistry, behavioural tests), preclinical therapy studies in mouse models, blood and CSF biomarker analysis, coordination and design of a phase II clinical study with Alzheimer’s disease patients (

Homepage Department/Research Group

Selected Recent Publications

  • Bayer TA (2015) Proteinopathies, a core concept for understanding and ultimately treating degenerative disorders? European Neuropsychopharmacology 25:713-724
  • Bayer TA & Wirths O (2014) Focusing the amyloid cascade hypothesis on N-truncated Abeta peptides as drug targets against Alzheimer?s disease. Acta Neuropathol. 127(6): 787-801
  • Wirths O, Bayer TA (2012) Intraneuronal Ab accumulation and neurodegeneration: Lessons from transgenic models. Life Sciences 91:1148-1152
  • Jawhar S, Wirths O, Bayer TA (2011) Pyroglutamate Abeta a hatchet man in Alzheimer disease. J. Biol. Chem. VOL. 286, NO. 45, pp. 38825?38832

Original Papers:

  • Dietrich K, Bouter Y, Müller M, Bayer TA (2018) Synaptic alterations in mouse models for Alzheimer Disease - a Special Focus on N-truncated Abeta 4-42. Molecules 23(4). pii: E718. doi: 10.3390/molecules23040718
  • Noguerola JSL, Giessen NME, Ueberück M, Meißner JN, Pelgrim C, Adams J, Wirths O, Bouter Y, Bayer TA (2018) Synergistic effect on neurodegeneration by N-truncated Aβ4-42 and pyroglutamate Aβ3-42 in a mouse model of Alzheimer’s Disease. Front. Aging Neurosci. 10:64 doi: 10.3389/fnagi.2018.00064
  • Storck SE, Meister S, Nahrath J, Meißner JN, Schubert N, Di Spiezio A, Baches S, Vandenbroucke RE, Bouter Y, Prikulis I, Korth C, Weggen S, Heimann A, Schwaninger M, Bayer TA and Pietrzik CU (2016) Endothelial LRP1 transports amyloid-? 1-42 across the blood-brain barrier. J. Clin. Invest. 126:123-36.
  • Antonios G, Borgers H, Richard BC, Brauß A, Meißner J, Weggen S, Pena V, Pillot T, Davies SL, Bakrania P, Matthews D, Brownlees J, Bouter Y, Bayer TA (2015) Alzheimer therapy with an antibody against N-terminal Abeta 4-X and pyroglutamate Abeta 3-X. Scientific Reports 5:17338 | DOI: 10.1038/srep17338
  • Bouter Y, Noguerola JSL, Tucholla P, Crespi GAN, Parker MW, Wiltfang J, Miles LA and Bayer TA (2015) Abeta targets of the biosimilar antibodies of Bapineuzumab, Crenezumab, Solanezumab in comparison to an antibody against N-truncated Abeta in sporadic Alzheimer disease cases and mouse models. Acta Neuropathol. 130(5)713-729.
  • Bouter Y, Kacprowski T, Weissmann R, Dietrich K, Borgers H, Brauß A, Sperling C, Wirths O, Albrecht M, Jensen LR, Kuss AW & Bayer TA (2014) Deciphering the molecular profile of plaques, memory decline and neuron-loss in two mouse models for Alzheimer?s disease by deep sequencing. Frontiers in Aging Neurosciences 6: 10.3389/fnagi.2014.00075
  • Bouter Y, Dietrich K, Wittnam JL, Rezaei-Ghaleh N, Pillot T, Papot-Couturier S, Lefebvre T, Sprenger F, Wirths O, Zweckstetter M, Bayer TA (2013) N-truncated amyloid ? (A?) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits. Acta Neuropathol. 126(2):189-205
  • Wittnam JL, Portelius E, Zetterberg H, Gustavsson MK, Schilling S, Koch B, Demuth H-U, Blennow K, Wirths O, Bayer TA (2012) Pyroglutamate Amyloid ß (Aß) Aggravates Behavioral Deficits in Transgenic Amyloid Mouse Model for Alzheimer Disease. J. Biol. Chem. 287 (11): 8154?8162
  • Jawhar S, Wirths O, Schilling S, Graubner S, Demuth HU, Bayer TA (2011) Overexpression of glutaminyl cyclase, the enzyme responsible for pyroglutamate abeta formation, induces behavioral deficits and glutaminyl cyclase knock-out rescues the behavioral phenotype in 5XFAD mice. Journal of Biological Chemistry 286(6):4454?4460
  • Wirths O, Erck E, Martens H, Harmeier A, Geumann C, Jawhar S, Kumar S, Multhaup G, Walter J, Ingelsson M, Degerman-Gunnarsson M, Kalimo H, Huitinga I, Lannfelt L, Bayer TA (2010) Identification of low molecular weight pyroglutamate Abeta oligomers in Alzheimer disease: a novel tool for therapy and diagnosis pyroglutamate Abeta oligomers in Alzheimer disease: a novel tool for therapy and diagnosis. Journal of Biological Chemistry 53:41517-24