Dr. Dan Ehninger

Group Leader

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

dan.ehninger(at)dzne.de
+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

A paternal methyl donor-rich diet altered cognitive and neural functions in offspring mice.

Ryan DP, Henzel KS, Pearson BL, Siwek ME, Papazoglou A, Guo L, Paesler K, Yu M, Müller R, Xie K, Schröder S, Becker L, Garrett L, Hölter SM, Neff F, Rácz I, Rathkolb B, Rozman J, Ehninger G, Klingenspor M, Klopstock T, Wolf E, Wurst W, Zimmer A, Fuchs H, Gailus-Durner V, Hrabě de Angelis M, Sidiropoulou K, Weiergräber M, Zhou Y, Ehninger D. Mol Psychiatry 2017, doi:10.1038/mp.2017.53. Work highlighted as Editor's Choice in Science Translational Medicine (9 (2017): 386).  

High-dose maternal folic acid supplementation before conception impairs reversal learning in offspring mice.

Henzel KS, Ryan DP, Schröder S, Weiergräber M, Ehninger D. Sci Rep 2017, 7:3098.  

SGPL1 (sphingosine phosphate lyase 1) modulates neuronal autophagy via phosphatidylethanolamine production.

Mitroi DN, Karunakaran I, Gräler M, Saba JD, Ehninger D, Ledesma MD, van Echten-Deckert G. Autophagy 2017, 13: 885-899.  

Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies.

Wagner J, Krauss S, Shi S, Ryazanov S, Steffen J, Miklitz C, Leonov A, Kleinknecht A, Göricke B, Weishaupt JH, Weckbecker D, Reiner AM, Zinth W, Levin J, Ehninger D, Remy S, Kretzschmar HA, Griesinger C, Giese A, Fuhrmann M. Acta Neuropathol 2015, 130:619-631.  

Limited effects of an eIF2αS51A allele on neurological impairments in the 5xFAD mouse model of Alzheimer's disease.

Paesler K, Xie K, Hettich MM, Siwek, Ryan DP, Schröder S, Papazoglou A, Broich K, Müller R, Trog A, Weiergräber M, Ehninger D. Neural Plast 2015:825157. Work highlighted on World Biomedical Frontiers.

Mechanism and treatment for learning and memory deficits in mouse models of Noonan syndrome.

Lee YS, Ehninger D, Zhou M, Oh JY, Kang M, Kwak C, Ryu HH, Butz D, Araki T, Cai Y, Balaji J, Sano Y, Nam CI, Kim HK, Kaang BK, Burger C, Neel BG, Silva AJ. Nat Neurosci 2014, 17:1736-43. Work highlighted by commentary in Nature Neuroscience (17:1627-9).

Bison: Bisulfite alignment on nodes of a cluster.

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

Longevity, aging and rapamycin.

Ehninger D, Neff F, Kan X. Cell Mol Life Sci 2014, 71:4325-46.

Rapamycin extends murine lifespan but has limited effects on aging.

Neff F, Flores-Dominguez D, Ryan DP, Horsch M, Schroder S, Adler T, Afonso LC, Aguilar-Pimentel JA, Becker L, Garrett L, Hans W, Hettich MM, Holtmeier R, Holter SM, Moreth K, Prehn C, Puk O, Racz I, Rathkolb B, Rozman J, Naton B, Ordemann R, Adamski J, Beckers J, Bekeredjian R, Busch DH, Ehninger G, Graw J, Hofler H, Klingenspor M, Klopstock T, Ollert M, Stypmann J, Wolf E, Wurst W, Zimmer A, Fuchs H, Gailus-Durner V, Hrabe de Angelis M, Ehninger D. J Clin Invest 2013, 123:3272-91. 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.

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, 77:647-54. Work highlighted by commentary in Nature Reviews Neuroscience (14:227).

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

Ehninger D. Neuropharmacology 2013, 68:97-105. Work highlighted as key article on Psychology Progress.

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, 17:62-70.

Rapamycin for treating Tuberous sclerosis and Autism spectrum disorders.

Ehninger D, Silva AJ. Trends Mol Med 2011, 17:78-87.

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, 107:13141-6.

Genetics and neuropsychiatric disorders: treatment during adulthood.

Ehninger D, Silva AJ. Nat Med 2009, 15:849-50.

Reversing neurodevelopmental disorders in adults.

Ehninger D, Li W, Fox K, Stryker MP, Silva AJ. Neuron 2008, 60:950-60.

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, 14:843-8. 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, 104:18280-5.

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, 27:1505-13.

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, 13:845-51. 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.

Significance

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.