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Zempel lab
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Zempel lab

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Principal investigator

Hans Zempel, MD PhD

Institut für Humangenetik
Kerpener Str. 34
50931 Köln (Cologne), Germany
Tel.: +49 221 478-86837

Fax: +49 221 478-86812

 

Group members
 

 

Group research focus

Our research group is broadly interested in the pathomechanism of neurodegenerative and rare genetic neurological diseases. In particular, we work on the identification and characterization of key factors that lead to impairment of neuronal and synaptic function. Rare diseases often give valuable insights also for the understanding and treatment of more common, age-related disorders like Alzheimer Disease.

 With additional support of the CMMC, our lab uses state of the art microscopic, cellular, genetic and biochemical tools in order to identify and characterize genetic and non-genetic causes of neurodegeneration of the central and peripheral nervous system.

 Our main research focus is on the cellular and molecular mechanisms and treatment of

  • Alzheimer Disease and related dementia & Tauopathies (e.g. Frontotemporal Dementia, Pick's Disease, Corticobasal Degeneration, Progressive Supranuclear Palsy)

  • Mitochondrial Depletion Syndromes (Polymerase Gamma deficiencies like Alpers Syndrome) and neurodegenerative diseases caused by impaired mitochondrial function

  • Neurologic disease related to impairment of cytoskeletal components or transport (e.g. Hereditary Spastic Paraplegia caused by SPAST/SP4, Lissencephalies caused by Tubulin based migration defects)

  • Neurologic disease linked to lysosomal storage diseases

  • Neuronal cell polarity

We are constantly looking for collaborators to expand our horizon. We welcome at any time initiatives for grant applications, cool science and the exchange of ideas on how to treat neurodegenerative diseases.

Link to publications listed in pubmed: https://www.ncbi.nlm.nih.gov/pubmed/?term=hans+zempel

 

Selected Publications

Zempel H, Dennissen FJA, Kumar Y, Luedtke J, Biernat J, Mandelkow EM, Mandelkow E.
Axodendritic sorting and pathological missorting of Tau are isoform-specific and determined by axon initial segment architecture.
J Biol Chem. 2017 Jul 21;292(29):12192-12207. doi: 10.1074/jbc.M117.784702. Epub 2017 May 23.

 

Zempel H, Sadzot B and Haag N.
Treatment Avenues for the Juvenile and Adult Onset Mitochondriopathies Alpers Syndrome, Ataxia Neuropathy Spectrum, MEMSA and PEO Caused by Polymerase-Gamma Mutations Ala467Thr and Trp748Ser.
SM J Neurol Neurosci. 2017; 3(2): 1013. Review.

 

Zempel H, Mandelkow EM.
Tau missorting and spastin-induced microtubule disruption in neurodegeneration: Alzheimer Disease and Hereditary Spastic Paraplegia.
Mol Neurodegener. 2015 Dec 21;10:68. doi: 10.1186/s13024-015-0064-1. Review.

 

Zempel H, Mandelkow E.
Lost after translation: missorting of Tau protein and consequences for Alzheimer disease.
Trends Neurosci. 2014 Dec;37(12):721-32. doi: 10.1016/j.tins.2014.08.004. Epub 2014 Sep 12. Review.

 

Zempel H, Luedtke J, Kumar Y, Biernat J, Dawson H, Mandelkow E, Mandelkow EM.
Amyloid-β oligomers induce synaptic damage via Tau-dependent microtubule severing by TTLL6 and spastin.
EMBO J. 2013 Nov 13;32(22):2920-37. doi: 10.1038/emboj.2013.207. Epub 2013 Sep 24.

 

Li X, Kumar Y, Zempel H, Mandelkow EM, Biernat J, Mandelkow E.
Novel diffusion barrier for axonal retention of Tau in neurons and its failure in neurodegeneration.
EMBO J. 2011 Oct 18;30(23):4825-37. doi: 10.1038/emboj.2011.376.

 

Timm T, von Kries JP, Li X, Zempel H, Mandelkow E, Mandelkow EM.
Microtubule affinity regulating kinase activity in living neurons was examined by a genetically encoded fluorescence resonance energy transfer/fluorescence lifetime imaging-based biosensor: inhibitors with therapeutic potential.
J Biol Chem. 2011 Dec 2;286(48):41711-22. doi: 10.1074/jbc.M111.257865. Epub 2011 Oct 7.

 

Zempel H, Thies E, Mandelkow E, Mandelkow EM.
Abeta oligomers cause localized Ca(2+) elevation, missorting of endogenous Tau into dendrites, Tau phosphorylation, and destruction of microtubules and spines.
J Neurosci. 2010 Sep 8;30(36):11938-50. doi: 10.1523/JNEUROSCI.2357-10.2010. Erratum in: J Neurosci. 2012 Apr 25;32(17):6052.

 

Miura Y, Sakurai Y, Hayakawa M, Shimada Y, Zempel H, Sato Y, Hisanaga S, Endo T.
Translocation of lysosomal cathepsin D caused by oxidative stress or proteasome inhibition in primary cultured neurons and astrocytes.Biol Pharm Bull. 2010;33(1):22-8.