Scope of the group: Acute and slowly degenerative diseases, such as stroke, Alzheimer’s disease (AD) and Parkinson’s disease are all without a cure and although etiologically very distinct, they share common pathological hallmarks. One of the main shared features of these diseases is neuroinflammation geared by activated glia. Instead of supporting neuronal connectivity as they do in the healthy brain, glial cells get activated, secrete neurotoxic molecules and contribute to neuronal malfunctions.   Understanding of glial functions, especially microglia and astrocytes and the interplay between peripheral inflammation and neuroinflammation is the key for development of therapeutics aimed at modulating inflammation for CNS benefit. We believe that proper engagement of beneficial microglial functions offers means to combat neurodegenerative diseases. Our research aims at finding not only disease specific but also common mechanism of neuroinflammation and how these can be taken advantage to modulate neuroinflammation for CNS benefit.

METHODOLOGICAL APPROACH: We use novel, human-based models to find new therapeutic targets for the disease benefit and to discover novel biomarkers. We develop new human iPSC-based models including microglia and immunocompetent organoids and use living human brain tissue biopsies. We investigate cellular responses using various omics approaches, electrophysiology and microscopy techniques.  In addition, we take advantage of animal modelling with functional outcomes. We utilize several both transgenic and surgically induced animal models of neurodegeneration, especially Alzheimer’s disease and stroke. We carry out research using APP/PS1 and 5XFAD mice to model Alzheimer’s disease and permanent and transient stroke models. The functional outcome is measured by using various behavioral tests with long term follow up time.