Neurosciences
Main Research: Neurosciences
Term: 01.01.2022 – 30.06.2024 (bonus time until 31.12.2024)
Alcoholism and depression are highly comorbid disorders. Neutral sphingomyelinase (NSM) is suggested as a missing link between emotional status and alcohol consumption due to the downstream effects on the serotoninergic system. A new line of mice with NSM gene knockout specifically in the brain serotoninergic system was created to investigate if the interaction between NSM and the brain serotoninergic system determines the comorbidity between negative emotional state and alcohol consumption.
PD Dr. Liubov Kalinichenko
Psychiatrische und Psychotherapeutische Klinik
Main Research: Neurosciences
Term: 01.12.2021 – 30.11.2024
Inflammatory bowel disease (IBD) predisposes for synucleinopathies like Parkinson Disease. This is putatively caused by propagation of chronic inflammation into the brain. The hypothesis of this project is that chronic inflammation in IBD activates microglia in distinct brain regions, thereby mediating neuronal pathology and aggravating synucleinopathy. This hypothesis will be tested in post mortem brain tissue of IBD patients and mice with colitis.
Dr. Patrick Süß
Neurologische Klinik
- Email: patrick.suess@uk-erlangen.de
Main Research: Neurosciences
Term: 01.01.2022 – 30.06.2024
Proper Schwann cell development and myelination are essential for a functional peripheral nervous system and regulated by networks of chromatin modifiers and transcription factors. Here I plan to study the role of the acetyltransferase Tip60 as part of the Tip60/Ep400 chromatin remodeling complex in lineage progression and myelination by characterizing its target genes and interaction with transcription factor Sox10. Results may help to better understand peripheral neuropathies.
Dr. Franziska Thiele
Institut für Biochemie
- Email: franziska.thiele@fau.de
Main Research: Neurosciences
Term: 01.10.2022 – 31.03.2025 (bonus time until 30.09.2025)
Reactive carbonyl species (RCS) are linked to development of metabolic syndrome including neuropathic pain and fatty liver disease (MAFLD), but the possibly synergistic role of RCS in both conditions remains to be investigated. This project aims at analyzing RCS as biomarkers in neuropathic pain patients with or without concomitant MAFLD, with parallelncomprehensive experimental neurophysiological examinations of patients and assessment of functional effects of RCS on sensory neurons in vitro.
Dr. Margareta Miriam Düll
Medizinische Klinik 1
- Email: miriam.duell@uk-erlangen.de
Main Research: Neurosciences
Term: 01.01.2024 – 30.06.2026
The aim of this project is to facilitate the understanding of the role of extracellular vesicles (EVs) in the development and progression of Parkinson’s disease (PD). EVs extracted from blood of PD patients and controls will be fractionated according to cellular origin and cargo profiling will be performed focusing on pathogenic forms of aSyn and regulatory RNAs. The results will offer deeper insights in PD-related signatures, and permit exploring the origin and transfer of pathogenic molecules.
Dr. Fanni Annamaria Boros
Molekular-Neurologische Abteilung
Main Research: Neurosciences
Term: not started yet
We aim to develop a voxelomic atlas of the brain. We will leverage high-resolution, multi-spectral ex-vivo imaging data from Magnetic Resonance Imaging (MRI) in combination with deep learning techniques, to compare single-voxel data between individuals. The atlas will serve as a tool to interpret single-voxel neuroanatomical variability. The project will build on preliminary work in sample preparation and data processing techniques.
Prof. Alexander German
Molekular-Neurologische Abteilung
Main Research: Neurosciences
Term: 01.06.2024 – 30.11.2026
Loss of spatacsin protein leads to the development of SPG11-HSP disorder. It has a rapid progression and exhibits various neurological symptoms, like Parkinsonism, and is characterized by dysregulated glycosphingolipid metabolism. The research examines the connection between SPG11 depletion, lysosomal glycosphingolipid degradation pathway and protein aggregation.
Dr. Daniil Kachkin
Stammzellbiologische Abteilung