Publications

@article{Bauer2025,

title = {Pragmatic algorithm for visual assessment of 4-Repeat tauopathies in [18F]PI-2620 PET Scans},

author = {Theresa Bauer and Matthias Brendel and Mirlind Zaganjori and Alexander M. Bernhardt and Alexander Jäck and Sophia Stöcklein and Maximilian Scheifele and Johannes Levin and Thilo van Eimeren and Alexander Drzezga and Osama Sabri and Henryk Barthel and Robert Perneczky and Günter Höglinger and Nicolai Franzmeier and Johannes Gnörich},

doi = {10.1016/j.neuroimage.2025.121001},

issn = {1053-8119},

year  = {2025},

date = {2025-02-00},

urldate = {2025-02-00},

journal = {NeuroImage},

volume = {306},

publisher = {Elsevier BV},

keywords = {Biomarker, Tau PET, Tauopathy},

pubstate = {published},

tppubtype = {article}

}

@article{Slemann2024,

title = {Neuronal and oligodendroglial, but not astroglial, tau translates to in vivo tau PET signals in individuals with primary tauopathies},

author = {Luna Slemann and Johannes Gnörich and Selina Hummel and Laura M. Bartos and Carolin Klaus and Agnes Kling and Julia Kusche-Palenga and Sebastian T. Kunte and Lea H. Kunze and Amelie L. Englert and Yunlei Li and Letizia Vogler and Sabrina Katzdobler and Carla Palleis and Alexander Bernhardt and Alexander Jäck and Andreas Zwergal and Franziska Hopfner and Sebastian N. Roemer-Cassiano and Gloria Biechele and Sophia Stöcklein and Gerard Bischof and Thilo van Eimeren and Alexander Drzezga and Osama Sabri and Henryk Barthel and Gesine Respondek and Timo Grimmer and Johannes Levin and Jochen Herms and Lars Paeger and Marie Willroider and Leonie Beyer and Günter U. Höglinger and Sigrun Roeber and Nicolai Franzmeier and Matthias Brendel},

doi = {10.1007/s00401-024-02834-7},

issn = {1432-0533},

year  = {2024},

date = {2024-12-00},

urldate = {2024-12-00},

journal = {Acta Neuropathol},

volume = {148},

number = {1},

publisher = {Springer Science and Business Media LLC},

abstract = {<jats:title>Abstract</jats:title><jats:p>Tau PET has attracted increasing interest as an imaging biomarker for 4-repeat (4R)-tauopathy progressive supranuclear palsy (PSP). However, the translation of in vitro 4R-tau binding to in vivo tau PET signals is still unclear. Therefore, we performed a translational study using a broad spectrum of advanced methodologies to investigate the sources of [<jats:sup>18</jats:sup>F]PI-2620 tau PET signals in individuals with 4R-tauopathies, including a pilot PET autopsy study in patients. First, we conducted a longitudinal [<jats:sup>18</jats:sup>F]PI-2620 PET/MRI study in a 4-repeat-tau mouse model (PS19) and detected elevated [<jats:sup>18</jats:sup>F]PI-2620 PET signals in the presence of high levels of neuronal tau. An innovative approach involving cell sorting after radiotracer injection in vivo revealed higher tracer uptake in single neurons than in the astrocytes of PS19 mice. Regional [<jats:sup>18</jats:sup>F]PI-2620 tau PET signals during the lifetime correlated with the abundance of fibrillary tau and with autoradiography signal intensity in PSP patients and disease controls who underwent autopsy 2–63 months after tau PET. In autoradiography, tau-positive neurons and oligodendrocytes with a high AT8 density, but not tau-positive astrocytes, were the drivers of [<jats:sup>18</jats:sup>F]PI-2620 autoradiography signals in individuals with PSP. The high tau abundance in oligodendrocytes at the boundary of gray and white matter facilitated the identification of an optimized frontal lobe target region to detect the tau burden in patients with PSP. In summary, neuronal and oligodendroglial tau constitutes the dominant source of tau PET radiotracer binding in 4-repeat-tauopathies, translating to an in vivo signal.</jats:p>},

keywords = {Signal sources, Tau PET, Tauopathy},

pubstate = {published},

tppubtype = {article}

}

@article{Langerscheidt2024,

title = {Genetic forms of tauopathies: inherited causes and implications of Alzheimer’s disease-like TAU pathology in primary and secondary tauopathies},

author = {Felix Langerscheidt and Tamara Wied and Mohamed Aghyad Al Kabbani and Thilo van Eimeren and Gilbert Wunderlich and Hans Zempel},

doi = {10.1007/s00415-024-12314-3},

issn = {1432-1459},

year  = {2024},

date = {2024-06-00},

urldate = {2024-06-00},

journal = {J Neurol},

volume = {271},

number = {6},

pages = {2992--3018},

publisher = {Springer Science and Business Media LLC},

abstract = {<jats:title>Abstract</jats:title><jats:p>Tauopathies are a heterogeneous group of neurologic diseases characterized by pathological axodendritic distribution, ectopic expression, and/or phosphorylation and aggregation of the microtubule-associated protein TAU, encoded by the gene <jats:italic>MAPT</jats:italic>. Neuronal dysfunction, dementia, and neurodegeneration are common features of these often detrimental diseases. A neurodegenerative disease is considered a primary tauopathy when <jats:italic>MAPT</jats:italic> mutations/haplotypes are its primary cause and/or TAU is the main pathological feature. In case TAU pathology is observed but superimposed by another pathological hallmark, the condition is classified as a secondary tauopathy. In some tauopathies (e.g. <jats:italic>MAPT</jats:italic>-associated frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and Alzheimer's disease (AD)) TAU is recognized as a significant pathogenic driver of the disease. In many secondary tauopathies, including Parkinson's disease (PD) and Huntington's disease (HD), TAU is suggested to contribute to the development of dementia, but in others (e.g. Niemann-Pick disease (NPC)) TAU may only be a bystander. The genetic and pathological mechanisms underlying TAU pathology are often not fully understood. In this review, the genetic predispositions and variants associated with both primary and secondary tauopathies are examined in detail, assessing evidence for the role of TAU in these conditions. We highlight less common genetic forms of tauopathies to increase awareness for these disorders and the involvement of TAU in their pathology. This approach not only contributes to a deeper understanding of these conditions but may also lay the groundwork for potential TAU-based therapeutic interventions for various tauopathies.</jats:p>},

keywords = {Genetics, Tauopathy},

pubstate = {published},

tppubtype = {article}

}

@article{Bischof2024,

title = {Improved Tau PET SUVR Quantification in 4-Repeat Tau Phenotypes with [^{18}F]PI-2620},

author = {Gérard N. Bischof and Matthias Brendel and Henryk Barthel and Hendrik Theis and Michael Barbe and Peter Bartenstein and Joseph Claasen and Adrian Danek and Günter Höglinger and Johannes Levin and Ken Marek and Bernd Neumaier and Carla Palleis and Marianne Patt and Michael Rullmann and Dorothee Saur and Matthias L. Schroeter and John Seibyl and Mengmeng Song and Andrew Stephens and Osama Sabri and Alexander Drzezga and Thilo van Eimeren},

doi = {10.2967/jnumed.123.265930},

issn = {2159-662X},

year  = {2024},

date = {2024-06-00},

urldate = {2024-06-00},

journal = {J Nucl Med},

volume = {65},

number = {6},

pages = {952--955},

publisher = {Society of Nuclear Medicine},

keywords = {Tau PET, Tauopathy},

pubstate = {published},

tppubtype = {article}

}