New thesis about resolution of inflammation in Alzheimer’s disease brain

Alzheimer’s disease (AD) is characterized by chronic inflammation due to excessive accumulation of proteins forming amyloid plaques and tangles in the brain. The inflammatory response is a process aiming to protect the host. However, unresolved inflammation and persistent immune system activation can result in tissue damage and cell death and, in the case of AD, ultimately memory deficits. The main focus of my thesis is to investigate the lipids and proteins involved in the resolution process to reveal changes occurring during the disease progression of AD, and to utilize the protective pro-resolving lipid mediators for terminating the inflammation in order to provide repair and homeostasis in AD.

Which are the most important results? 

Our studies showed that proteins and lipids involved in the resolution of inflammation are altered in human AD brains and in a mouse model for AD, indicating disruption of this process. These factors were changed in an age-dependent manner in the AD mouse model, suggesting the importance of timing for stimulating resolution. Importantly, we demonstrated that pro-resolving lipid mediators given exogenously to the mouse AD model resulted in rescuing memory functions.

How can this new knowledge contribute to the improvement of people’s health? 

This thesis shows the potential of using the pro-resolving lipid mediators as a therapeutic strategy to stimulate resolution of the chronic inflammation in AD and thereby provide beneficial effects on cognitive functions.

What´s in the future for you? Will you keep on conducting research? 

I have always been intrigued by neurodegenerative diseases and wanted to help people by finding new therapeutic strategies. This could have a big impact on the affected patients. I would like to continue working in the field of neuroscience.