Neurodegenerative Disease Laboratory (Neudis)


>Late onset neurodegenerative diseases like Alzheimer’s and Parkinson’s disease are characterized by the build-up of specific protein aggregates in the degenerating cells. Rare families highlight the pathogenic importance of the aggregation process where mutations in the genes encoding the aggregation prone proteins cause autosomal dominant diseases. Aggregation of the protein alpha-synuclein (AS) in nerve and glial cells is the hallmark of the diseases Parkinson disease, Lewy body dementia, multiple systems atrophy and Lewy body variant of Alzheimer disease. Besides the aggregation per se are specific AS phosphorylations involved in disease promoting/preventing pathways. Key issues in the field centers around what forms of AS are toxic and how they impact the cells; the existence of disease protective pathways suffering due to environmental or genetic predispositions; selective vulnerability factors among individuals and cell populations; identification of early disease manifestations (biomarkers).

Our research focus on characterizing pathogenic mechanisms in synucleinopathies and using them in modeling the diseases in cells and animals the aim of contributing to development of neuroprotective strategies. This is done using a wide range of biochemical, molecular and cell biological techniques on cell, animal and human specimens including genomics and proteomics in close collaboration with national and international collaborators in academia, funding agencies and industry.

Research interests

  • Factors that trigger AS aggregation and Serine 129 phosphorylation. This includes search for AS aggregation inducing factors like the protein p25? and kinases screens.
  • Cytotoxic mechanisms initiated by AS aggregation and Serine129-phosphorylation. This includes specific interactions with vital cellular factors formed by AS upon aggregation as well as transcription inducing signal cascades. Current targets are molecules involved in ion homeostasis, cytoprotective and transcription factors.
  • Protective pathways preventing the development of AS aggregates and their toxicity with a current focusing on kinases and NF-kB modulated pathways
  • Disease modeling in transgenic cell line models, primary neurons and oligodendrocytes  from transgenic mice,in vivo modeling using transgenic mice expressing human AS and our own conditional human p25?/TPPP transgenic mice
  • Biomarkers of AS dependent neurodegeneration with current activity aiming at disease associated transcriptional response and development of AS aggregate specific antibodies.
  • Biology of p25?/TPPP protein in relation to brain disorders


  • Molecular biology, cloning, mutagenesis, vector construction.
  • Quantitative mRNA analysis, qPCR, gene array analysis.
  • Prokaryotic protein expression and purification.
  • Antibody generation. We have year-long experience in making and characterizing antibodies against misfolded AS species. This is currently part of biomarker projects
  • Protein aggregation, amyloid formation, oligomer formation.
  • Protein chemistry, proteome analysis
  • Cell biology, immunofluorescense microscopy, generation of stable cell lines, gene silencing, plate reader analysis, cellular calcium imaging, small scale screening of aggregate and kinase inhibitors.
  • Transgenic mice breeding and characterization. We have generated a conditional LoxP/stop/LoxP-p25? transgenic mice and are studying the effect of expressing this protein in oligodendrocytes and neurons. The mice are crossed with mice expressing human a-synuclein in the brain to investigate the effect of p25? on a-synuclein aggregation in vivo.
  • Immunohistochemistry of mice and human brain

Collaborators and centres

  • Neurocampus Aarhus
  • FP7 - Neurasync Academic-Industrial Training Network on Alpha-synuclein-related Brain Diseases.
  • FP7 - European Project on Mendelian Forms of Parkinson’s Disease (MEFOPA)
  • Danish Innovation Consortium CureND, Consortium expired 2010
  • Nordic Centre of Excellence in Molecular Neurodegeneration, Center expired 2009
  • Prof. Glenda Halliday, Brain and Mind Institute, University of Sydney, Australia
  • Prof. Jing Zhang, Division of Neuropathology, University of Washington School of Medicine, USA
  • Senior Scientist Wei-Ping Gai, Department of Human Physiology, Flinders University, Australia
  • Prof. Michael Lee, Institute for Translational Neuroscience, University of Minnesota, USA
  • Prof. Deniz Kirik, Department of Experimental Medical Science, Lund University, Sweden
  • Prof. Eliezer Masliah, Department of Neurosciences, University of California, San Diego, USA
  • Prof. Philipp Kahle, Hertie Institute for Clinical Brain Research, Tübingen, Germany
  • Prof. Tiago F. Outeiro, Center of Molecular Physiology of the Brain, University of Göttingen, Germany
  • Prof. Daniel Otzen, Dept. Molecular Biology, Aarhus University
  • Assoc. prof., Marina Romero-Ramos, Dept. Biomedicine, Aarhus University

Research group members

Group leader

Poul Henning Jensen

H bldg. 1171, 420
P +4587167793
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