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Laura Airas


Dr Laura Airas is currently Associate Professor and lecturer in neurology at the University of Turku, Finland. She is also a consultant in neurology at Turku University Hospital. Since 2000, she has acted as a principal investigator on industry-sponsored interventional MS-studies.

She received her medical training at University of Turku, Finland, where she was also awarded a PhD. Her doctorate included an internship at Glaxo Institute of Molecular Biology, Geneva, Switzerland.

Dr Airas’ research activities focus on unravelling the cause of neurodegeneration in multiple sclerosis (MS). Her specific interests center on improving techniques to visualize disease-related diffuse atrophy, with the aim of identifying patients with progressive MS and improving their treatment.

Role of microglia in the pathogenesis of progressive multiple sclerosis

Conventional magnetic resonance imaging (MRI) techniques are currently the cornerstone of multiple sclerosis (MS) diagnostics and clinical follow-up. MRI is sensitive in demonstrating focal inflammatory lesions and diffuse atrophy. However, in patients with progressive MS, there is increasingly widespread diffuse pathology outside the plaques that is often related to microglial activation and neurodegeneration. This cannot be detected using conventional MRI.

Positron emission tomography (PET) imaging, using the 18 kDa translocator protein (TSPO), which binds radioligands, has recently shown promise as a tool to detect this compartmentalized pathology in vivo, allowing its development to be followed longitudinally. It is becoming evident that the more advanced the MS disease is, the more widespread is microglial activation, and it is likely that microglial activation is also functionally related to neurodegeneration. PET imaging can be performed both in animal models of MS and in patients with MS, thus allowing detection of MS progression-related pathology at a molecular level in vivo. Microglial cells appear in numerous phenotypes but can robustly be subdivided into M1-like pro-inflammatory cells or M2-like debris-clearing cells. Our hypothesis is that by promoting microglia transition from M1- to M2-type, neurodegeneration could be reduced, thus slowing down disease progression.

Our specific aim is to try and identify, using TSPO-PET, those patients with relapsing-remitting MS who have a high burden of microglial activation and who are thus more likely to enter the progressive phase of the disease. In addition, we aim to search for compounds that can modulate the microglial cell phenotype and use them for treatment of chronic experimental autoimmune encephalitis (EAE) in rodents. The EAE outcome will be evaluated clinically and by in vivo micro-PET imaging. Analysis of microglial cell phenotype will be done ex vivo/in situ. Our studies aim to pave the way for personalized treatment of progressive MS. 

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