Michael Heneka, University of Bonn, Germany

Michael Heneka


1996    Medical degree (with excellence), University of Tübingen
1998    Dr.med. (summa cum laude), University of Tübingen, Germany
2002    Board examination for Clinical Neurology, University of Bonn, Germany
2003    Habilitation, University of Bonn, Germany

Research and Professional Experience:

2003 –2004     Senior Clinical Fellow, Dept. of Neurology, University of Bonn
2004 –2008     Prof. of Molecular Neurology (C3), Dept. of Neurology, University of Münster
since 2008       Prof. of Clinical Neurology (W3), Dept. of Neurology, University of Bonn
since 2010       Member of the German Center for Neurodegeneration (DZNE)
since 2010       Head of the Neurodegeneration Outpatient Unit (KBFZ)
since 2013       Adjunct Professor, Dept. of Medicine, University of Massachusetts
since 2016      Chair, Dept. of Neurodegenerative Disease and Geriatric Psychiatry, University of Bonn,

Awards and Honours:

1992 –1996     Fellow of the Studienstiftung des Deutschen Volkes
1999                Attempto Award, University of Tübingen
2011                Christa-Lorenz Award for ALS Research
2013                Hans und Ilse Breuer Alzheimer Research Award

Research Focus

Heneka has always been interested in immunology and neuroscience. At the very beginning of his career Heneka combined his experimental knowledge in immunology with questions arising from the field of neuroscience and in particular neurodegenerative disease. In a second line of his research, Heneka showed that the degeneration of the locus coeruleus and subsequent changes of norepinephrine levels in its hippocampal and cortical projection areas, facilitate and promote innate immune reactions upon deposition of fibrillar beta-amyloid in murine alzheimer disease models. Recently, I demonstrated that inhibition of NLRP3-mediated immune activation protects APP/PS1 mice from the development of amyloid pathology, spine loss and decline of learning and memory. Furthermore, we found that  apoptosis-associated speck-like proteins containing a CARD (ASC) released by microglia, bind rapidly to amyloid-β and increase the formation of amyloid-β oligomers and aggregates, acting as an inflammation-driven cross-seed for amyloid-β pathology.

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Supporting Publications
Organised by
  • Elsevier
  • TLP
  • TLN
  • Encephalitis Society
  • Treating Autism
  • Encephalitis Society
  • Treating Autism