Dr. Dan Ehninger

Group Leader

German Center for Neurodegenerative Diseases (DZNE)
Sigmund-Freud-Str. 27 
53127 Bonn

+49 (0) 228 / 43302-530
+49 (0) 228 / 43302-538 (Secretary)

Group members

Name Phone
Almana Mukabenova, Assistant +49 (0) 228 / 43302-538
Dr. Brandon Pearson, Postdoc +49 (0)228/43302-533
Dr. Kan Xie, Postdoc +49 (0)228/43302-531
Kristin Henzel, PhD Student +49 (0)228/43302-532
Astrid Markert, Technical Assistant +49 (0)228/43302-533

Selected Publications

Mechanism and treatment for the learning and memory deficits associated with mouse models of Noonan syndrome.

Lee YS, Ehninger D, Zhou M, Oh JY, Butz D, Araki T, Nam CI, J Balaji, Sano Y, Amin A, Kim HK, Burger C, Neel BG, Silva AJ. Nat Neurosci. 2014 Dec;17(12):1736-43.

Bison: Bisulfite alignment on nodes of a cluster.

Ryan DP, Ehninger D. BMC Bioinformatics. 2014 Oct 18;15:337.

Longevity, aging and rapamycin.

Ehninger D, Neff F, Kan X. Cell Mol Life Sci. 2014 Jul 12.

Rapamycin extends lifespan but has limited effects on aging in mice.

Neff F, Flores-Dominguez D, Ryan DP, Horsch M, Schröder S, Adler T, Caminha Afonso L, Aguilar-Pimentel JA, Becker L, Garrett L, Hans W, Hettich MM, Holtmeier R, Hölter S, Moreth K, Prehn C, Puk O, Rácz I, Rathkolb B, Rozman J, Naton B, Ordemann R, Adamski J, Beckers J, Bekeredjian R, Busch DH, Ehninger G, Graw J, Höfler H, Klingenspor M, Klopstock T, Ollert M, Stypmann J, Wolf E, Wurst W, Zimmer A, Fuchs H, Gailus-Durner V, Hrabě de Angelis M, Ehninger D. J Clin Invest. 2013 Aug 1;123(8):3272-91. Work highlighted by news article in Science (342 (2013): 789), as well as commentaries in the Journal of Clinical Investigation (123(8) (2013): 3204-6) and Aging (Albany NY) (5(8) (2013):592-8). See also Faculty of 1000 Prime evaluation.

From genes to cognition in tuberous sclerosis: Implications for mTOR inhibitor-based treatment approaches.

Ehninger D. Neuropharmacology. 2013 May;68:97-105.  

mTOR Inhibition ameliorates cognitive and affective deficits caused by Disc1 knockdown in adult-born dentate granule neurons.

Zhou M, Li W, Huang S, Song J, Kim JY, Tian X, Kang E, Sano Y, Liu C, Balaji J, Wu S, Zhou Y, Zhou Y, Parivash SN, Ehninger D, He L, Song H, Ming GL, Silva AJ. Neuron. 2013 Feb 20;77(4):647-54.  

Gestational immune activation and Tsc2 haploinsufficiency cooperate to disrupt fetal survival and may perturb social behavior in adult mice.

Ehninger D, Sano Y, de Vries PJ, Dies K, Franz D, Geschwind DH, Kaur M, Lee YS, Li W, Lowe JK, Nakagawa JA, Sahin M, Smith K, Whittemore V, Silva AJ. Mol Psychiatry. 2012 Jan;17(1):62-70.

Rapamycin for treating Tuberous sclerosis and Autism spectrum disorders.

Ehninger D, Silva AJ. Trends Mol Med. 2011 Feb;17(2):78-87.

Neurofibromin regulates corticostriatal inhibitory networks during working memory performance.

Shilyansky C, Karlsgodt KH, Cummings DM, Sidiropoulou K, Hardt M, James AS, Ehninger D, Bearden CE, Poirazi P, Jentsch JD, Cannon TD, Levine MS, Silva AJ. Proc Natl Acad Sci U S A. 2010 Jul 20;107(29):13141-6.

Genetics and neuropsychiatric disorders: treatment during adulthood.

Ehninger D, Silva AJ. Nat Med. 2009 Aug;15(8):849-50.

Reversing neurodevelopmental disorders in adults.

Ehninger D, Li W, Fox K, Stryker MP, Silva AJ. Neuron. 2008 Dec 26;60(6):950-60.

Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis.

Ehninger D, Han S, Shilyansky C, Zhou Y, Li W, Kwiatkowski DJ, Ramesh V, Silva AJ. Nat Med. 2008 Aug;14(8):843-8. Work highlighted by news article in Science (323(5911) (2009): 203-5), Nature Reviews Neuroscience research highlight (9 (2008): 582-3) and Faculty of 1000 Biology & Medicine evaluations.

Specific developmental disruption of disrupted-in-schizophrenia-1 function results in schizophrenia-related phenotypes in mice.

Li W, Zhou Y, Jentsch JD, Brown RA, Tian X, Ehninger D, Hennah W, Peltonen L, Lönnqvist J, Huttunen MO, Kaprio J, Trachtenberg JT, Silva AJ, Cannon TD. Proc Natl Acad Sci U S A. 2007 Nov 13;104(46):18280-5. 

Physical exercise prevents age-related decline in precursor cell activity in the mouse dentate gyrus.

Kronenberg G, Bick-Sander A, Bunk E, Wolf C, Ehninger D, Kempermann G. Neurobiol Aging. 2006 Oct;27(10):1505-13. 

Regional effects of wheel running and environmental enrichment on cell genesis and microglia proliferation in the adult murine neocortex.

Ehninger D, Kempermann G. Cereb Cortex. 2003 Aug;13(8):845-51. See also Faculty of 1000 Biology evaluation.

Curriculum Vitae

Dan Ehninger studied medicine in Berlin from 1997 to 2003. From 2001 to 2004, he carried out his medical thesis in the laboratory of Gerd Kempermann at the Max Delbrück Center for Molecular Medicine in Berlin, where he worked on the behavioral regulation of adult hippocampal neurogenesis and adult cell formation in the neocortex. His postdoctoral work (2004 to 2009) with Alcino Silva at University of California - Los Angeles (Departments of Neurobiology, Psychiatry & Biobehavioral Sciences, Psychology and the Brain Research Institute) focused on molecular and cellular mechanisms of cognitive impairments in mouse models of neuropsychiatric disorders. Since 2010, Dan Ehninger is group leader at the DZNE in Bonn.


Areas of investigation/research focus

The group is interested in the neurobiological mechanisms that underlie learning and memory formation under physiological conditions. Additionally, our research efforts focus on pathophysiological mechanisms relevant for cognitive impairments in the context of aging and neuropsychiatric disorders. We use an interdisciplinary research approach based on methods of mouse genetics, behavioral neuroscience, molecular biology and biochemistry, neuroanatomical analyses and neurophysiological studies.


The complexity of the brain is reflected in the number of synapses between individual cells. It is estimated that the number of synapses in the human brain is approximately 1014. During synaptic plasticity, which is fundamental for learning and memory formation, neurons have the capability to shape the length, structure and distribution of synapses in order to refine local activity. Unfortunately, during pathological conditions, including neurodegenerative disorders such as Alzheimer’s disease, uncontrolled large-scale loss of synapses triggers local neuronal degeneration. Thus, loss of connectivity compromises neuronal activity and destabilizes neuronal information processing, which is a key determinant in the onset of cognitive decline. Understanding the pathways involved in the non-physiological dendritic spine remodeling will help to prevent excessive synaptic pruning and therefore will aid in the development of a cure against cognitive impairments associated with aging and neurodegenerative conditions.