Our research

Our research focuses on identifying new early mechanisms and biomarkers associated with Alzheimer's disease (AD) and thereby improve the development of new treatments and diagnostic tools. Our strategy is to investigate the effect of AD risk factors like stress, inflammation, metabolic changes, and amyloidogenesis, on different types of brain cells including pericytes, astrocytes, neurons, and NG2 cells. We use a translational approach where our hypotheses are built upon postmortem brain observations. These are followed up by in vitro experiments and studies on human CSF and plasma. This approach has revealed several new mechanisms and biomarkers associated with AD, including alteration of glycogen metabolism, the toxicity of various amyloid peptides aggregation forms, and secretion of a variety of pathology-specific molecules.

Aims

• Understand the role of amyloid peptides (including amyloid-beta, IAPP, TDP-43) in blood-brain barrier (BBB) alterations and how it affects the progression of AD.

Impact

We aim to distinguish and understand different pathways that fuel AD progression in humans. The gained knowledge will hopefully help clinicians to provide correct information on diagnosis, treatment, and disease progression. Moreover, it may push the development of individual tailor-made therapeutic interventions forward.

How our research contributes to the goals of MultiPark

We aim to fulfil Multiparks goals by exploring novel AD mechanisms and investigating how aggregated amyloid peptides affect brain function and cell integrity. Our work also spans from human brain tissue and cohort studies to in vitro and animal studies which is line with Multiparks translational initiative. Our research addresses the aim of MultiPark's working group 1.

Research Team & Publications

Our group is a specific subgroup within a larger context of clinical memory research.

Read about publications and research team members of the Clinical Memory Research in the LU Research Portal.