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ePoster
HYPOXIA AS POTENTIAL REGULATOR OF INFLAMMATION IN PARKINSON’S DISEASE
Rebecca Kotzurand 3 co-authors
University of Veterinary Medicine Hannover
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-328
Presentation
Date TBA
Board: PS05-09AM-328
Event Information
Poster Board
PS05-09AM-328
Poster
View posterAbstract
Parkinson’s disease (PD) is the second most common neurodegenerative disease with high burden on patients and caregivers, but lack of disease modifying treatment. Therefore, identification of a common denominator and cause for initiation and progression of this disease are research priorities. It is widely accepted, that the pathogenic aggregation of the alpha synuclein (aSyn) protein is involved in the loss of dopaminergic neurons in PD. In this project, we aim to illuminate the influence of hypoxia on the progression and initiation of PD in a murine model with focus on inflammation. Activity of immune cells is altered by the degree of hypoxia in tissue, and hypoxia was previously shown to contribute to neurological diseases. We hypothesize that aSyn pathology and the resident hypoxia pathways influence each other.
We will analyze the immune cells’ composition in an animal model displaying aSyn pathology (line 61, Thy1-aSyn mice) and characterize alterations of neuronal activity in primary neuronal cultures from these mice w/wo hypoxia factoring in the duration of hypoxia (acute/chronic). Additionally, we are not only investigating the brain but are also incorporating the whole body of the mice to allow assumptions regarding the spread, perpetuation and initiation of PD from the brain to the gut and vice versa. Currently, we are establishing a hypoxia model in primary neuron.
For our future studies, we will focus on the influence of these observed reactions towards the hypoxic stress on the interaction of the neuronal cells with immunological relevant cells like microglia.
We will analyze the immune cells’ composition in an animal model displaying aSyn pathology (line 61, Thy1-aSyn mice) and characterize alterations of neuronal activity in primary neuronal cultures from these mice w/wo hypoxia factoring in the duration of hypoxia (acute/chronic). Additionally, we are not only investigating the brain but are also incorporating the whole body of the mice to allow assumptions regarding the spread, perpetuation and initiation of PD from the brain to the gut and vice versa. Currently, we are establishing a hypoxia model in primary neuron.
For our future studies, we will focus on the influence of these observed reactions towards the hypoxic stress on the interaction of the neuronal cells with immunological relevant cells like microglia.
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