Doctoral Candidate Position 7 - University of Aarhus, Denmark
Identify the disease relevant molecular pathways in peripheral monocytes during Parkinson's disease development
Huajing is a Marie-Curie PhD Fellow at the Department of Biomedicine, Aarhus University. His
main supervisor is Prof. Marina Romero-Ramos. His research focuses on the interaction between
central and peripheral immune mechanisms in Parkinson's disease, with a particular interest in how
monocytes and T cells contribute to the progression in PD across different disease stages and
between sexes.
Before joining Aarhus University, Huajing earned his master's degree in Anaesthesiology from
Zhejiang University. He mainly focused on the role of the zona incerta in consciousness and
anaesthetic-induced cognitive impairment during his master studies. His background bridges
systems neuroscience, molecular biology, and computational analysis, driving his goal to connect
fundamental mechanisms with clinical applications in neurodegeneration.
Currently, he aims to employ single-cell transcriptomics to characterize immune signatures across
PD subtypes and integrates multi-omics data to link molecular signatures with cellular function.
Through collaborations within the BICEPs network, his project aims to identify biomarkers and
therapeutic targets modulating immune activity in Parkinson's disease.
University Profile Huajing Cai
ORCID: 0009-0000-9424-7706
Description of project
Parkinson's disease (PD) is the fastest growing neurodegenerative disease and as today it has no cure. Research data supports an important role for the immune cells in brain and periphery in PD, and suggest the chronic inflammation observed in patients contribute to the PD neuronal loss. To explore possible immunomodulatory targets in peripheral cells we will use novel data that the lab has obtained from single cell RNA sequencing of peripheral blood monocytes from people with different PD suptype sand at differnet disease stages. Differentially regulated genes will be validated by analysis of monocytes in different PD patient cohorts by conventional flow and PCR. Moreover, we will evaluate the potential of differentially regulated genes to modify monocyte physiology and their response to disease relavant α-synuclein using cell cultures approaches. Since T-cells have been shown to influence neuronal death in PD, we will study how this modification will affect monocytes and dendritic cells to interact with T cells activating adaptive immunity after exposure to α-synuclein. Selected targets will also be tested in vivo by using transgenic or knock-out mice and/or immunomodulatory drugs where α-synuclein PD neurodegeneration will be modelled. We will evaluate adaptive immunity, immune cell migration to brain, neurodegeneration, and neuroinflammation. The project integrates techniques from in vivo modelling, and cell culture, histology and advanced microscopy, flow cytometry and other single cell techniques providing a multidisciplinary approach to investigating immune regulation in PD. Ultimately, this work could lead to the identification of novel drugs that modulate, offering potential new avenues for treating PD and related disorders.