Felix Winter

In-vivo regulation of Aβ abundance / Energy-metabolism and brain imaging in AD
"I am interested in the aethiopathology of the Alzheimer's disease."

Protein aggregation is a major hallmark of many neurodegenerative diseases. In Alzheimer's disease (AD) the deposition of the protein Amyloid-β (Aβ) is increased and its aggregation leads to cognitive impairment. The question we focus on is: Which mechanisms govern the production and degradation of Aβ inside the brain? How can these mechanisms be influenced to impede or delay disease progression? Which of these mechanisms can be attributed to the process of aging?

Neurodegenerative diseases like AD mostly occur at older ages. If it is possible to understand the underlying mechanisms, this may shed light on the question "What does `getting old` mean in a biological sense?".

We established a mathematical model to capture the in vivo dynamics of Aβ aggregation in mouse-models relating to the regulation of different transmembrane transport proteins. Based on this model the influence on different strategies of altering the Aβ, abundance on AD initiation can be examined. Once the key features of AD progression are worked out we will analyse their relation to aging.

Understanding the aethiopoathology of Alzheimer's disease and working out the inherent connection to the process of aging observed in biological organisms promises insights important for both basic aging research and questions specific for the treatment of the Alzheimer's disease.