I am working at the Institute of Molecular Medicine on the following project:
Human HSC aging and immunosenescence
I´m a member of the Department of Neurology under the supervision of Francesco Roselli. Studying the connectivity between the motor cortex and hypothalamus in an Amyotrophic Lateral Sclerosis transgenic mouse model will be my project for the next years. To have a rest I like to make music or I free my mind by riding racing bike.
My project focuses on the role of immunosenescence in altering alpha synuclein aggregation and spreading with ageing and in neurodegenerative disease like Parkinson’s disease. In my spare time, I like to spend time with my friends, read, or travel.
I am working in the lab of Prof. Schirmbeck on induction and regulation of vaccine-induced CD8 T-cell responses in aging mice.
Tamara Bang Tam Phan
I am working in the lab of Sebastian Iben on the Investigation of the pathomechanism in Trichothiodystrophy. Trichothiodystrophy (TTD) is an autosomal recessive premature aging disorder characterized by neuroectodermal symptoms and sulfur-deficient brittle hairs and nails. To date, mutations in the subunits of the transcription factor IIH (TFIIH) including XPB, XPD and p8/TTDA, and TFIIE including TFIIE beta are causing TTD. Due to the photosensitive form of TTD and the defect in the nucleotide excision repair (NER) pathway, TTD is suspected to be caused by DNA repair defects. However, patient with a non-photosensitive from of TTD and an intact NER pathway indiate a DNA repair -independent pathomechanism in TTD. Due to the dual function of TFIIH in the NER pathway and in basal transcription, I am investigating the basal transcription - dependent pathomechanisms in TTD.
Heike Katrin Schreier
The nuclear and the mitochondrial genome are constantly exposed to genotoxic injuries entailing DNA repair and replication blockage. Accumulation of DNA damage and replication stress in the nucleus as well as mitochondrial DNA instability have been associated with organismal aging.
In my PhD thesis under the supervision of Prof. Dr. Lisa Wiesmüller in the Section of Gynecological Oncology I want to gain further insights into how EndoG, a nuclear-encoded endonuclease with primary localization in mitochondria, links mitochondrial DNA metabolism and replication stress responses in the nucleus and investigate its impact on aging.
I am a PhD student in the Institute of Molecular Virology. The focus of the project is to understand the Interplay between HIV infection and Aging. I aim to elucidate the mechanisms involved in accelerated aging in HIV-1-infected individuals and critical for increased inflammation, immune damage and apoptosis in HIV-infected elderly individuals.
In my leisure time, I love to travel, spend time with friends and family. I enjoy cooking and I like to do sports.
I am a PhD student in the Institute of Physiological Chemistry. My project focuses on the role of astrocytic redox imbalance in brain aging, organismic aging and neurodegenerative diseases in CNS. In my free time, I like to play basketball.
As a PhD student in the Institute of Experimental Cancer Research, I am investigating how clonal hematopoiesis and changes in the epigenetic landscape upon aging of hematopoietic stem cells might pave the way for the development of acute myeloid leukemia.
Short description of my project (AG Danzer)
Non-fibrillar alpha-synuclein oligomers are most probably the toxic species in Parkinson’s Disease (PD). The aim of my project is to investigate the influence of aging on alpha-synuclein oligomerization and the development of a PD phenotype with a view on motoric, histological, biochemical and cell biological characteristics. Although, aging is the major risk factor for PD, it is not known whether the length of time or the point in time is decisive for the development of the disease. I am comparing motor functions and the accumulation of oligomers in transgenic mice exhibiting long and constant expression levels of alpha-synuclein, with mice expressing alpha-synuclein in higher age but only for a short time period. Furthermore, we want to investigate the influence of age-dependent increased activity of the RhoGTPase Cdc42 and alpha-synuclein oligomerization. CASIN which is an inhibitor of Cdc42 will be used for a systemic treatment of alpha-synuclein transgenic mice to study its effects on oligomerization, reorganization of neurons and the development of motoric symptoms in this PD mouse model.