Partners
Partner 1.
Neuronal Survival Unit, Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, BMC A10, 221 84 Lund, Sweden. (Coordinator)
The Neuronal Survival Unit was formed in 1995. The research is focused on neuronal stem cells, neurogenesis in the adult brain and intracerebral transplantation in attempts to repair brains in animal models of Parkinson, Huntington and Alzheimer diseases. We also study pathogenetic mechanisms and pharmacological treatments in cell and animal models of Huntington disease.
Partner 2.
Disease Modelling, Neurobiology, Wallenberg Neuroscience Center, Department of Experimental Medical Science, BMC A10, SE-221 84 Lund, Sweden.
The Disease modelling group is focused on disease modeling using recombinant AAV vectors to overexpress disease-causing proteins in the brain of rodents and primates. Using this approach Kirik has been able to develop a new model of PD, in both rats and primates, based on targeted overexpression of a-synuclein in the pars compacta of the substantia nigra.
Partner 3.
Laboratory for Experimental Brain Research, Wallenberg Neuroscience Center, Department of Clinical Neuroscience, BMC A13, 221 84 Lund, Sweden.
Stroke is the leading cause of long-term disability and the third leading cause of death in Sweden. The only approved stroke therapy is thrombolysis, limited to patients with embolic stroke and that must be initiated within three hours after symptoms. There is no approved neuroprotective therapy or therapy that enhances functional recovery after stroke or trauma. Evidently there is an urgent need for research that can establish such therapies. We have established in vivo and in vitro rodent models of cerebral ischemia, trauma and oxygen glucose deprivation, respectively. Using these models, we study the cellular and molecular mechanisms of cell death, cell repair and recovery of brain function.
Partner 4.
Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
Degradation of intracellular regulatory proteins is a tightly controlled process that is of pivotal importance for cells. The UPS is responsible for degradation of these regulatory proteins and in addition keeps the cellular environment clean from misfolded and aggregation-prone proteins. A broad array of human pathologies is characterized by the presence of deposits of misfolded proteins. These disorders include many neurodegenerative disorders like Alzheimer's, Huntington's, and Parkinson's disease as well as non-neurological disorders. We use our model systems to study the functional status of the UPS in these pathologies and identify factors that compromise the UPS. Our main objective is to understand the role of the ubiquitin/proteasome system (UPS) in human diseases, in particular in neurodegenerative disorders and cancer. In addition, we would like to understand why some UPS substrates resist or even hinder proteasomal degradation.
Partner 5.
Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
The Notch signalling pathway is a highly evolutionarily conserved mechanism for cell-cell communication, and plays a critical role in differentiation of most tissues in multicellular organisms. Given its prominent role in the decision between maintenance of a stem/progenitor state or progression towards more differentiated fates, mutations in the Notch pathway are linked with disease. A major focus of our laboratory is to learn how Notch integrates with other major signalling mechanisms.
Partner 6.
Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.
Aging is considered an important co-factor in several neurodegenerative diseases (ND), however, the link(s) between aging-dependent changes and the progression of NDs remains enigmatic. Neurodegeneration occurs in normal aging and sculpts the aged phenotype. Like many ND diseases aging-dependent neurodegeneration affects select groups of neurons while others are spared suggesting distinct pathological processes rather than diffuse global alterations. In the context of NCoE in molecular medicine -neurodegeneration, our goal is to understand if accumulation of (mitochondrial and nuclear) DNA modifications plays a role in aging-dependent neurodegeneration.
Partner 7.
Department of Neuroscience and Neurology, University of Kuopio, Finland.
Our major research interests are the identification of novel risk genes in Alzheimer's disease by means of molecular genetics and functional characterization of candidate genes involved in Alzheimer's disease in vitro and in vivo. We also work on the genetic and functional role of UBQLN1 in Alzheimer's disease and molecular genetics of other neurodegenerative diseases.
Partner 8.
Institute of Medical Biochemistry, University of Aarhus, Aarhus, Denmark.
During the last decade, our group has investigated the neurodegenerative processes in the synucleinopathies with a focus on the role played by a-synuclein modifications and its aggregation on cellular integrity on in vivo functionality. We search for factors and study signaling pathways e.g. posttranslational modifications that govern the pathogenecity of a-synuclein and its specific functional characteristics, e.g. solubility and protein interactions. Our aim is to develop models of neurodegenerative diseases and processes that can be used to develop novel neuroprotective and neurorestorative therapies.
Partner 9.
H Lundbeck A/S, Copenhagen, Denmark.
Partner 10.
Institute of Basal Medical Sciences and Centre for Molecular Biology and Neuroscience, University of Oslo, Norway.
Our group is interested in brain function, from molecules to behavior. We study fundamental principles and mechanisms of neuronal signalling in the mammalian brain, and the roles of ion channels in behaviour, brain function, and disease. We focus on the functions of ion channels, in particular K+ channels, in central neurons and circuits, mainly in the hippocampus and cerebral cortex. Methods: Electrophysiological and optical recordings in brain slices and in vivo, molecular genetic and pharmacological manipulations, computational modelling, and behavioural tests.
Partner 11.
Centre for Molecular Biology and Neuroscience, The National Hospital, Department for Medical Microbiology, Section for Molecular Biology, 0027 Oslo, Norway.
Repair of DNA damage is essential for protection against cancer and other age related diseases. DNA damage generated by ionizing radiation, simple alcylating agents or endogenously hydrolytic and oxidative processes is corrected by the base excision repair (BER) pathway(s). We are currently using two different approaches for the identification of new genefunctions for DNA repair. Our goal is to identify and characterize genfunctions required for genomic stability and for protection against cancer. Targeted mutations of DNA repair genes in mice.
Partner 12.
Laboratory of Molecular Brain Research, A.I. Virtanen Institute for Molecular Sciences, University of Kuopio, Kuopio, Finland.
The Laboratory of Molecular Brain Research investigates inflammatory mechanisms of neurodegeneration focusing on models of three different diseases, stroke (acute neurodegeneration), Alzheimer's disease and amyotrophic lateral sclerosis (chronic neurodegenerative diseases). We use several animal models of the diseases and utilize genetically modified mouse strains and cells both in vivo and in vitro. The idea is to investigate the role of key (inflammatory or cell death-promoting) enzymes at the molecular and cellular level and verify their significance in pathogenesis of the animal models of the brain diseases. Eventually, we try to obtain information from the human material of these diseases to understand the clinical relevance of these key enzymes.