Dr Raphael Hesse

Personal profile

• 2013 – 2017   PhD student at Boehringer Ingelheim / Ulm University BioCenter (BIU), Ulm, Germany

Research

Synaptic decline mediated by oligomeric Amyloid beta (Abeta) is thought to be the initial step in pathophysiology of Alzheimer’s disease (AD). To understand the cellular mechanisms of AD it is crucial to unravel how synapse loss is mediated as the disease proceeds. During my PhD I investigated synaptic signaling molecules in cerebrospinal fluid of AD patients and primary neuronal cell cultures, to study the association of synapse loss with disease progression. To further characterize how synapse loss is mediated in AD patients, I now focus on synaptic receptors as potential effectors of AD progression. By using cutting edge techniques, such as array tomography, hIPS cells and unbiased proteomic approaches, I want to identify synaptic receptors interacting with Abeta in human (derived) tissue and stem cells. Furthermore, I will test potential pharmacological interventions to reduce Abeta induced disturbances in calcium homeostasis and subsequent synaptotoxicity.

Recent publications

• Hesse R, Lausser L, Gummert P, Schmid F, Wahler A, Schnack C, Kroker KS, Otto M, Tumani H, Kestler HA, Rosenbrock H and von Arnim CA. (2017) Reduced cGMP levels in CSF of AD patients correlate with severity of dementia and current depression. Alzheimers Res Ther. 9;9(1):17. doi: 10.1186/s13195-017-0245-y.
• Hesse R, Wahler A, Gummert P, Kirschmer S, Otto M, Tumani H, Lewerenz J, Schnack C and von Arnim CA. (2016) Decreased IL-8 levels in CSF and serum of AD patients and negative correlation of MMSE and IL-1β. BMC Neurol. 26;16(1):185.