Prof. Dr. Dr. Jens Pahnke, EFN
Cooperation Unit Leader
Prof. Dr. Dr. Pahnke is head of the Neurodegeneration Research Lab (NRL)
German Center for Neurodegenerative Diseases (DZNE)
Leipziger Str. 44, House 15, Room 333
39120 Magdeburg
jens.pahnke@dzne.de
+49 (0) 391 / 67-24514
+49 (0) 391 / 67-24519 (Office)
+49 (0) 391 / 67-24528
| Name | Phone |
| Dr. Markus Krohn, Research Associate | +49 (0)391/67-24519 |
| Thomas Brüning, Technical Assistant | +49 (0)391/61-17168 |
Prof. Jens Pahnke is head of the Research Laboratory for Neurodegenerative Diseases (NRL) and the mouse house at the Center for Neurology. Since 2005, he is professor of neurodegeneration at the University of Rostock.
He graduated in medicine and human biology at the University of Greifswald. At Greifswald earned his doctorate in 2000 as MD at the medical faculty. Ongoing he spent a year as postdoc at the Clinic of Neurology of the Center for Neurology at the University of Rostock. Then Prof. Pahnke joined the Department of Pathology at the University Hospital Zurich (USZ). He earned his second doctorate in 2004 in the field of molecular biology. Since 2005, Prof. Pahnke teaches at the University of Rostock. He is an expert in the field of the function of blood-brain barrier transport molecules, specific mitochondrial mutations and new mouse models for studying the formation of protein aggregates in neurodegenerative diseases.
In 2008, he became the first German who was elected the "European Fellow of Neuropathology (EFN)” and received in 2009 the Research Award of the Alzheimer's Association Research Initiative
Professor Pahnke is member of the editorial boards of the Journal of Alzheimer's Disease (JAD), Frontiers in Neurodegenerative Diseases and Frontiers in Alzheimer's Disease and of the Grant Reviewing Board of the Alzheimer's Association.
At the DZNE site Magdeburg, Prof. Pahnke conducts the biomarker and autopsy studies and translational basic research projects.
ABC transporters B1, C1 and G2 differentially regulate neuroregeneration in mice
Schumacher T, Krohn M, Hofrichter J, Lange C, Stenzel J, Steffen J, Dunkelmann T, Paarmann K, Fröhlich C, Uecker A, Plath AS, Sommer A, Brüning T, Heinze HJ, Pahnke J. PLoS One. 2012;7(4):e35613. Epub 2012 Apr 24.
Mitochondrial DNA polymorphisms specifically modify cerebral β-amyloid proteostasis.
Scheffler K, Krohn M, Dunkelmann T, Stenzel J, Miroux B, Ibrahim S, von Bohlen und Halbach O, Heinze HJ, Walker LC und Gsponer JA, Pahnke J. Acta Neuropathol. 2012 Aug;124(2):199-208. Epub 2012 Apr 18.
Cerebral amyloid-β proteostasis is regulated by the membrane transport protein ABCC1 in mice.
Krohn M, Lange C, Hofrichter J, Scheffler K, Stenzel J, Steffen J, Schumacher T, Brüning T, Plath AS, Alfen F, Schmidt A, Winter F, Rateitschak K, Wree A, Gsponer J, Walker LC, Pahnke J. J Clin Invest. 2011 Oct;121(10):3924-31. doi: 10.1172/JCI57867. Epub 2011 Sep 1.
Determination of spatial and temporal distribution of microglia by 230nm-high-resolution, high-throughput automated analysis reveals different amyloid plaque populations in an APP/PS1 mouse model of Alzheimer's disease.
Scheffler K, Stenzel J, Krohn M, Lange C, Hofrichter J, Schumacher T, Brüning T, Plath AS, Walker L, Pahnke J. Curr Alzheimer Res. 2011 Nov;8(7):781-8.
Development of Alzheimer-disease neuroimaging-biomarkers using mouse models with amyloid-precursor protein-transgene expression.
Teipel SJ, Buchert R, Thome J, Hampel H, Pahnke J. Prog Neurobiol. 2011 Dec;95(4):547-56. Epub 2011 May 12.
Automated detection of amyloid-β-related cortical and subcortical signal changes in a transgenic model of Alzheimer's disease using high-field MRI.
Teipel SJ, Kaza E, Hadlich S, Bauer A, Brüning T, Plath AS, Krohn M, Scheffler K, Walker LC, Lotze M, Pahnke J. J Alzheimers Dis. 2011;23(2):221-37.
Evaluation of systemic targeting of RET oncogene-based MTC with tumor-selective peptide-tagged Ad vectors in clinical mouse models.
Schmidt A, Eipel C, Fürst K, Sommer N, Pahnke J, Pützer BM. Gene Ther. 2011 Apr;18(4):418-23. Epub 2011 Jan 13.
No evidence for THAP1/DYT6 variants as disease modifiers in DYT1 dystonia.
Kamm C, Uflacker N, Asmus F, Schrader C, Wolters A, Wittstock M, Pahnke J, Gasser T, Volkmann J, Münchau A, Hagenah J, Benecke R, Klein C, Lohmann K. Mov Disord. 2011 Sep;26(11):2136-7. doi: 10.1002/mds.23777. Epub 2011 Jun 2.
Periphilin is a novel interactor of synphilin-1, a protein implicated in Parkinson's disease.
Soehn AS, Franck T, Biskup S, Giaime E, Melle C, Rott R, Cebo D, Kalbacher H, Ott E, Pahnke J, Meitinger T, Krüger R, Gasser T, Berg D, von Eggeling F, Engelender S, da Costa CA, Riess O. Neurogenetics. 2010 May;11(2):203-15.
E2F1 Determines Human Melanoma Progression and Metastasis via EGF Receptor Signaling.
Alla V, Engelmann D, Niemetz A, Pahnke J, Schmidt A, Kunz M, Emmrich S, Steder M, Koczan D, Pützer BM (2010). J Natl Cancer I Jan 20;102(2):127-33.
Alzheimer's disease and blood-brain barrier function-Why have anti-beta-amyloid therapies failed to prevent dementia progression?
Pahnke J, Walker LC, Scheffler K, Krohn M. Neurosci Biobehav Rev. 2009 Jul;33(7):1099-108. Epub 2009 May 27.
Die Funktion der Blut-Hirn-Schranke für die Pathogenese der Alzheimer Demenz – Implikationen für immunologische Therapien zur Plaqueauflösung [The role of blood-brain barrier in the pathogenesis of Alzheimer dementia--implications for immunological therapies for plaque dissolution].
Pahnke J, Krohn M, Scheffler K. Fortschr Neurol Psychiatr. 2009 Aug;77 Suppl 1:S21-4. Epub 2009 Aug 14.
A complete list of publications can be found here.
Areas of investigation/research focus
Our basic research section focuses on new pathomechanisms of neurodegenerative disease (correlation of aging, mitochondrial dysfunction and beta-amyloid export), the establishment of mouse models and the discovery of new pharmaceutical components for the treatment of AD and PD. A central role for the accumulation of amyloid-beta play the blood-brain and the brain-CSF bariers. We investigate the function of export proteins (ABC transporters) for the specific export contribution and as future treatment options. We also established new mouse models expressing specific mitochondrial mutations to investigate their effect on amlyoid-beta load, microglial and ABC transporter function and the connection between aging and the accumulation of mitochondrial polymorphisms in neurodegerative diseases.
The clinical section focuses on the detection of amyloid-beta using NIR technologies, the prospective brain donation program and the discovery of new biomarkers in CSF/blood.
The cooperation partner's homepage can be found here.
