Jörg Hanrieder

Jörg Hanrieder

University of Gothenburg, Sweden

Jörg Hanrieder


Jörg Hanrieder is an Associate Professor of Neurobiology and a Group Leader in Analytical Neurochemistry. He earned his master’s degree in chemistry from the University of Leipzig, Germany, and subsequently completed his Ph.D. in Chemistry at Uppsala University, Sweden.

Currently holding the position of Associate Professor of Neurobiology at the University of Gothenburg, Sweden, Jörg Hanrieder plays a pivotal role in the Department of Psychiatry and Neurochemistry. Additionally, he is an Honorary Senior Research Fellow at the Department of Neurodegenerative Disease, Queen Square Institute of Neurology, UCL, London, UK.

His expertise lies in Molecular Neuroscience and analytical techniques. His research projects focus on Amyloid Pathology imaging, establishing him as an expert in Alzheimer's disease research. He is recognized as an expert in mass spectrometry, utilizing various innovative approaches.

Description of the general focus of the symposium "Molecular profiling of neurodegenerative disorders"

Alzheimer's disease (AD) presents a significant challenge in the field of neurodegenerative disease research, representing the most prevalent cause of dementia and contributing to over 60% of all dementia cases. Dementia, characterized by a decline in cognitive functions such as reasoning, memory, and speech, profoundly impacts the daily life of affected individuals. The disease is characterized by the accumulation and aggregation of misfolded proteins into intra- and extracellular deposits. This symposium aims to illuminate the elusive pathological mechanisms inherent in AD, with a particular emphasis on the transformation of beta-amyloid (Aβ) from a non-toxic monomer to a neurotoxic oligomeric species, ultimately leading to nerve cell death and cognitive decline. Additionally, the symposium will address the role of another key protein, tau, in Alzheimer's pathology. Tau, a microtubule-associated protein, undergoes abnormal phosphorylation in AD and forms neurofibrillary tangles (NFTs). The intricate interplay between Aβ and tau will be explored, shedding light on how their aggregation contributes to neuronal dysfunction and cognitive impairment. The symposium will delve into molecular imaging techniques, including mass spectrometry, hyperspectral imaging, and spatial transcriptomics, tailored for understanding plaque and tangle pathology. Invited speaker Jörg Hanrieder, an Associate Professor in Neurochemistry affiliated with the University of Gothenburg and University College London, will share insights from his expertise in neurochemistry and cutting-edge research on complex processes in neurodegenerative diseases. The discussion will encompass the aggregation dynamics of beta-amyloid (Aβ) peptides, unveiling the maturation process from diffuse plaques to cored plaques. Moreover, innovative approaches to tracking plaque age and correlating it with transcriptomic changes will be covered, providing insights into how genes respond to new plaques and how these responses evolve as plaques age. The integration of hyperspectral chemical imaging tools has facilitated the exploration of tangle polymorphisms in postmortem brain tissue. The discussion will include the characterization of the chemical phenotype to unravel the correlation between plaque and tangle characteristics and the progression of AD pathology, ultimately influencing cognitive decline.


"Mass Spectrometry based Molecular Imaging for Following Alzheimer’s Disease Pathology in Space and Time"

Mass spectrometry has gained increasing prominence in biomedical research providing as new apogee of molecular imaging. The technique combines features of molecular histology with the high dimensionality and specificity warranted by mass spectrometry at low um resolution. Our group has been advancing MS imaging approaches for chemical neuroimaging, specifically to understand neurodegenerative disease pathomechanisms.

Here, it is of critical importance to our understanding of Alzheimer’s disease (AD) pathology, to determine how key pathological factors including beta-amyloid (Aβ) plaque formation are interconnected and implicated in nerve cell death, clinical symptoms, and disease progression. Exactly how Aβ plaque formation begins and how the ongoing plaque deposition proceeds and initiates subsequent neurotoxic mechanisms is not well understood. The primary aim of our research is to elucidate the biochemical processes underlying early Aβ plaque formation in brain tissue.

We developed a chemical imaging pardigm including hyperspectral microscopy and mass spectrometry imaging that allows to delineate vivo Aβ build up and deposition at cellular length scales. Specifically, we advanced the integration of conformation sensitive hyperspectral mass spectrometry with MSI modalities to elucidate plaque morphology associated changes in Aβ signatures. We further pioneered means for amyloid chronology based on imaging stable isotope labelling kinetics (iSILK). Here, novel genetic AD mice are labelled metabolically with stable isotopes to follow the fate of aggregating Aβ species from before and throughout the earliest events of precipitating plaque pathology. This allowed to visualize Aβ aggregation dynamics within single plaques across different brain regions. We show that formation of structurally distinct plaques is associated with differential Aβ peptide deposition. These data, for the first time, describe a detailed picture of the earliest events of precipitating amyloid pathology at scales not previously possible.

The results from these studies bring considerable novel information about the deposition mechanism of Aβ and its toxic interactions with the surrounding. This will open up for developing tailored strategies to affect AD pathology prior to any neurodegenerative mechanisms as well as to develop new biomarkers for AD.

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