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Jensen Group

Jensen Group - Neurodegenerative Disease Laboratory

Our group is interested in understanding how alpha-synuclein contributes to the neurodegenerative processes in Parkinson’s disease, Lewy body dementia and multiple systems atrophy, which are hallmarked by the development of intracellular aggregates of alpha-synuclein. This is investigated in studies of alpha-synuclein aggregates in vitro, in cell models, transgenic animals and human tissue and involves development of new aggregate selective tools.

Research focus

The aim is to decipher how cells regulate their pools of alpha-synuclein species and how they respond to misfolded alpha-synuclein with respect to cytotoxic and protective mechanisms that can be targeted by therapy. This involves proteostatic mechanisms like autophagy, unconventional secretion, prion-like intercellular propagation and homeostatic cellular mechanisms being offset by alpha-synuclein aggregates.

Currently specific projects focuses on alpha-synucleins role in calcium regulation, kinase pathways regulating alpha-synuclein turn-over and toxicity, relation to the innate immune system and implementation of a mouse model for prion-like spreading of alpha-synuclein brain pathology.

Available projects

The Jensen group currently has projects available for Master and PhD students. Please contact Group Leader Poul Henning Jensen directly, if interested.


Previous news from the research group


2017.01.27 | People

Cristine Betzer is new assistant professor in Jensen group

Cristine Betzer has been appointed as assistant professor for 5 years in group leader Poul Henning Jensens group starting January 17th 2017. Cristine Betzer will be working towards understanding the disease causing mechanisms underlying alpha-synuclein aggregation induced cell death with specific focus on changes in different ion homeostasis.…

2016.11.11 | Research news

Poul Henning Jensen and Mark Denham received the Danish Parkinsons association Grant

Mark Denham got a grant for the project "Combining stem cells and novel bioactive scaffolds to develop new Parkinson Disease therapies" while Poul Henning Jensens project is called "Can caffeine treatment rescue alfa-synuclein aggregation dependent disease spreading and neuron loss? Investigating a novel neuroprotective principle in…

2015.02.18 | Research news

New publication from Poul Henning Jensen's - Phosphorylated a-synuclein in Parkinson's disease: correlation depends on disease severity

Phosphorylation of a-synuclein on serine 129 is closely linked to Parkinson’s disease. This clinical study critically studies the relation of phosphorylated a-synuclein to parkinson’s disease progression and symptomatology using more defined patient cohorts. The study was lead by our collaborator prof. Jing Zhang, University of Washington.

2015.02.09 | Research news

New publication from Poul Henning Jensen's group - Identification of Synaptosomal Proteins Binding to Monomeric and Oligomeric alpha-Synuclein

In this proteomic study we have identified those proteins in nerveterminals (synaptosomes) that preferentially bind to alpha-synuclein in its normal monomeric and its pathological oligomeric states. The study was conducted in collaboration with prof. Jing Zhang, University of Washington.

2014.06.27 | Research news

New publication from Poul Henning Jensen's group - DJ-1 interactions with alpha-synuclein attenuate aggregation and cellular toxicity in models of Parkinson's disease

Alpha-synuclein and DJ-1 are key players in Parkinson disease possessing opposing effects with alpha-synuclein harming and DJ-1 protecting cells. We found that DJ-1 directly interact with alpha-synuclein thereby attenuating its toxic effect. The study is in collaboration with University Medical Center Göttingen and University of Leicester.

2014.06.06 | Research news

New publication - How epigallocatechin gallate can inhibit alpha-synuclein oligomer toxicity in vitro

New publication from Poul Henning Jensen's group in collaboration with prof. Daniel Otzen's group at iNANO published in The Journal of Biological Chemistry. This study investigated how the flavonoid epigallocatechin gallate protects against alpha-synuclein oligomer cytotoxicity that forms in Parkinson's disease.

2014.03.24 | Research news

New publication - Accumulation of oligomer-prone alpha-synuclein exacerbates synaptic and neuronal degeneration in vivo

New publication from Poul Henning Jensen's group published in Brain, a Journal of Neurology. Results from this study support the hypothesis that accumulating oligomeric alpha-synuclein may mediate early synaptic pathology in Parkinson's disease and dementia with Lewy bodies by disrupting synaptic vesicles. This oligomer-prone model might be useful…

2013.12.17 | Research news

New publication - Prodegenerative IkBalpha expression in oligodendroglial alpha-synuclein models of multiple system atrophy

New publication from Poul Henning Jensen's group published in Journal of Neurobiology of Disease. Multiple system atrophy (MSA) is a progressive, neurodegenerative disease characterized by parkinsonism, ataxia, autonomic dysfunction, and accumulation of alpha-synuclein in oligodendrocytes. Favoring oligodendroglial NF-kB activation may represent a…

2013.12.11 | Research news

New publication - Characterizing the dynamics of alpha-synuclein oligomers using hydrogen/deuterium exchange monitored by mass spectrometry

New publication from Poul Henning Jensen's group published in Journal of Biochemistry. Soluble oligomers formed by alpha-synuclein (alphaSN) are suspected to play a central role in neuronal cell death during Parkinson's disease. In this study, the structural dynamics of soluble alphaSN oligomers was analyzed using hydrogen/deuterium exchange…

2013.10.10 | Research news

New publication from Poul Henning Jensen's group - Structural and functional characterization of two alpha-synuclein strains

New results published in Nature Communications on the structure and function of two polymorphs of alpha-synuclein, a protein implicated in a number of neurological diseases such as for example Parkinson and dementia.

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