Topic: Parkinson’s disease

Study cellular mechanisms of Parkinson’s disease in the Jan Lab. Research integrates patient genetics, genomics and biomarkers with cellular and animal models, functional-genomic screening and measurements of morphology and transcription. Fellows develop independent projects during a three-year programme with a possible fourth year.

Investigate and validate therapeutic targets for Parkinson’s disease through neuronal and glial models, including iPSC-derived cells and co-cultures. Design cellular and biochemical experiments to clarify mechanisms of action and translate findings into drug-discovery decisions. The advertised salary range is USD 143,000–173,250. The exact role page currently accepts applications and does not state a fixed closing date.

Neurons in the cortico-basal ganglia circuit become excessively synchronised at beta frequencies (15-35 Hz) in Parkinson’s disease. However, it is unclear how this synchronised firing evolves across the network. Beta synchrony has often been assumed to emerge homogenously across the neurons within anatomical structures of the basal ganglia. However, it is possible that beta oscillations may emerge in a modular fashion within the neurons that make up an anatomical structure. We hypothesized that neurons in subregions of the basal ganglia preferentially reflect onset and offset of beta oscillati

Parkinson’s Disease (PD) is a neurodegenerative disorder associated with the loss of dopaminergic neurons in the nigrostriatal circuit, and the development of motor and non-motor symptoms. Currently, no disease-modifying pharmacological treatments are available, and dopamine-based therapies help to mitigate symptoms but also cause side-effects. In this context, indirect evidence has suggested that activation of metabotropic Glutamate Receptor 3 (mGluR3) exerts neuroprotective effects in animal models of PD. However, the lack of selective agonists/ligands for this receptor has hindered more in-

Dopamine (DA) neurons in the substantia nigra are vital for the control of movement. This fundamental function is encoded by the output signal of DA neurons which switches from spontaneous firing to bursts of action potentials. The latter produces an increase of DA release in targeted areas which is associated to locomotion initiation. The impairment of this process, such as DA neurons degeneration, leads to the motor symptoms of Parkinson’s disease. The activation of the N-methyl-D-aspartate receptors (NMDARs), by the simultaneous binding of glutamate and a co-agonist, is indispensable for th

The striatum is densely innervated by midbrain dopamine (DA) neurons but also receives a further sparse monoaminergic innervation by raphe serotonin (5-HT) neurons. Striatal 5-HT has been suggested to have some opposing functions to DA but also to regulate DA release which might support (or counteract) this functional antagonism. We explored the reciprocal modulation of electrically evoked striatal DA and 5-HT release and the underlying cell circuits by using fast-scan cyclic voltammetry to detect DA, a new G-protein-coupled receptor sensor for 5-HT (GRAB5-HT3.0) and whole-cell recordings in a