Alzheimer’s disease (AD) is characterized by pathological protein aggregation and aberrant immune responses in the brain, ultimately leading to neurodegeneration and cognitive decline. The APOE-e4 genotype represents the strongest genetic risk factor for AD, yet the mechanisms through which it shapes immune responses in the human brain remain poorly understood.
This PhD project aims to uncover how genetic risk influences immune cell function in AD by integrating single-nucleus epigenomic profiling of brain immune cells with high-resolution spatial transcriptomics. The PhD candidate will characterize epigenetic and transcriptional states of immune cells in post-mortem human brain tissue and map these states in relation to disease pathology in AD tissue. In parallel, immune responses will be modeled in human stem cell–derived systems to identify regulatory mechanisms driving immune dysfunction.
The PhD candidate will work closely with computational and experimental researchers and receive training in neuroimmunology, neurodegenerative disease research, and advanced spatial and single-cell technologies within a collaborative and multidisciplinary research environment. The project also offers opportunities to engage in international collaborations and present findings at scientific meetings.
We are looking for a motivated candidate with:
- a master’s degree in molecular or cellular biology, neuroscience, biomedical sciences, or a related field;
- a strong interest in neurobiology and immunology;
- affinity with, or experience in, single-cell or spatial transcriptomics;
- experience with epigenetic approaches is an advantage;
- good oral and written communication skills in English is required;
- the ability to work both independently and collaboratively within a team.
