Portrait Craig Garner

Prof. Dr. Craig Garner

Group Leader

German Center for Neurodegenerative Diseases (DZNE)
c/o Charité – Universitätsmedizin Berlin
Charitéplatz 1
10117 Berlin

+49 (0) 30 / 450-539166
+49 (0) 30 / 450-539916

Group members
Name Phone
Dr. Frauke Ackermann, Postdoc +49 (0) 30 / 450 - 639173
Sheila Hoffmann, PhD Student +49 (0) 30 / 450 - 539185
Christine Bruns, Technical Assistant +49 (0) 30 / 450 - 539185
Anny Kretschmer, Technical Assistant +49 (0) 30 / 450 - 639173
Katharina Schneider, Postdoc +49 (0) 30 / 450 - 639173
Curriculum vitae

Craig Garner studied Biochemistry at Purdue University in the USA and worked as postdoctoral fellow at the Friedrich Miescher Institute in Basel. In 1988 he became a group leader at the Center for Molecular Neurobiology in Hamburg (ZMNH) and continued his career at the University of Alabama in Birmingham. In 2002, he became Nancy Pritzker Professor at Stanford University in California and since 2003 he has co-directed the Down syndrome Center at Stanford University. Craig Garner is a well known expert in translational research and received several prices for his work, among those are the „Coulter Foundation Award for Translational Neuroscience“, the „Fidelity Foundation Award for Neurodegenerative Research“ and the „Stanford Neuro-Innovation Award for Translational Neuroscience“.  Moreover, Craig Garner has co-founded two small biotech companies: „Stealth Bioscience Inc.“ and “Balance Therapeutics Inc.“ The primary objective of the Stealth program is to develop new nanotechnologies that support intracellular recordings of neuronal cells using solid-state devices. The goal of the Balance program is to develop rational pharmacotherapies to normalize cognition in individuals with Down syndrome. The “Compose21” clinical trial is current evaluating a first set of candidate drugs. Within the DZNE Craig Garner will continue his research on the pathophysiology of synaptic dysfunction as it relates to neurodegenerative disorder with the goal of translating concepts developed from basic research into viable clinical treatment.

Selected publications

Usp16 contributes to somatic stem-cell defects in Down's syndrome.

Adorno, M., et al. (2013). Nature 501(7467): 380-384.

Bassoon and Piccolo regulate synaptic vesicle pool size and synapse integrity by regulating the E3 ubiquitin ligase Siah1.

Waites, C.L., Leal-Ortiz, S., Ng, P., Fejtova, A., Altrock, W., Gundelfi nger, E.D. and C.C. Garner. EMBOJ. 2013; 32:954-969.

Autism associated mutations in ProSAP2/Shank3 impair synaptic transmission and neurexin/neuroligin mediated transsynaptic signaling.

Arons, M., Thynne, C., Grabrucker, A.M., Li, D., Schön, M., Cheyne, J.E. Boeckers, T.M. Montgomery,J.M. and C.C. Garner. J Neuroscience. 2012; 32:14966–14978.

Piccolo regulates the dynamic assembly of presynaptic F-actin.

Waites, C.L., Leal-Ortiz, S., Andlauer, T.F., Sigrist, S.J., and C.C. Garner. J Neuroscience. 2011; 31(40):14250-63.

Synaptic SAP97 isoforms regulate AMPA receptor dynamics and access to presynaptic glutamate.

Waites, C.L., Specht, C. G., Haertel, K., Leal-Ortiz, S., Li, D., Drisdel, R.C., Jeyifous, O, Genoux, D., Cheyne, JE., Green, W.N., Montgomery, J.M.* and C.C. Garner*. J of Neuroscience. 2009; 29, 4332- 4345.

Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome.

Fernandez F, Morishita W, Zuniga E, Nguyen J, Blank M, Malenka RC, and C.C. Garner. Nat Neurosci. 2007; 10:411-413.

Unitary assembly of presynaptic active zones from Piccolo-Bassoon transport vesicles.

Shapira, M,, Zhai, R.G., Dresbach, T., Bresler, T., Torres, V.I., Gundelfi nger, E.D., Ziv, N.E., and C.C. Garner. Neuron. 2003; 38(2): 237-52.

Assemblying the presynaptic active zone: Characterization of an Active zone precursor vesicle.

Zhai, R., Friedmon, H.V. Cases-Langhoff, C., Beckers, B., Gundelfi nger, E.D, Ziv, N.*, and C. C. Garner. Neuron. 2001; 29:131-143.

SAP102, a novel postsynaptic protein that binds the NMDA receptor NR2 subunits.

Müller, B.M., U. Kistner, S. Kindler, W.J. Chung, S. Kuhlendahl, L-F. Lau, R.W. Veh, R.L. Huganir, E.D. Gundelfinger, and C.C. Garner. Neuron. 1996; 17:255-265.

SAP90, a rat presynaptic protein related to the product of the Drosophila tumor suppressor gene dlg-A.

Kistner, U., B. Wenzel, R. Veh, C. Cases-Langhoff, U. Appeltauer, E.D. Gundelfi nger, and C.C. Garner. J. Biol. Chem. 1993; 268(7):4580-4583.

Selective localization of messenger RNA for cytoskeletal protein MAP2 in dendrites.

Garner, C.C., R. Tucker and A. Matus. Nature. 1988; 336:674-677.

The complete list of publications is found here.

Areas of investigation/research focus

The work of my group is focused on understanding the molecular, cellular and physiological mechanisms regulating the dynamic assembly and function of vertebrate CNS synapses. Much of the early work of my group was designed to identify and characterize core components of excitatory synapses and define which roles they play in the regulated release of neurotransmitters and the dynamic recruitment, retention and function of postsynaptic glutamate receptors. These studies have shown that cellular programs that control the dynamic exchange and degradation of pre- and postsynaptic proteins govern the formation, maintenance and integrity of synapses.  Ongoing work in the lab is focused on how genetic and/or environmental insults adversely influence these programs, leading to synapse dysfunction and/or neuronal degeneration.

My group is also interested in translating our acquired knowledge on synapse dynamics and function to the development of pharmacotherapies to restore cognitive impairment in both neurodevelopmental and neurodegenerative disorders.  As one example, studies on mouse models of Down syndrome have shown that excessive inhibitory tone within neuronal circuits can lead to cognitive impairment, a condition that can be reversed by administering low doses of a variety of GABAA receptor antagonists.  Intriguingly, excessive inhibitory tone also appears to contribute to cognitive dysfunction in monogenic forms of autism as well as patients with Alzheimer’s disease.  These observations suggest that strategies aimed at modulating inhibitory tone may have broad therapeutic value.  To test this concept, we founded a small biotech company, “Balance Therapeutics Inc.” in 2009.  This organization recently initiated a phase Ib/II clinical trial (Compose 21) to assess whether modulating inhibitory tone can restore cognitive function in young adults with Down syndrome and eventually individuals with Alzheimer’s disease.