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Hans Zempel

Researcher at University of Cologne

Publications -  31
Citations -  1772

Hans Zempel is an academic researcher from University of Cologne. The author has contributed to research in topics: Tau protein & Axon initial segment. The author has an hindex of 11, co-authored 27 publications receiving 1429 citations. Previous affiliations of Hans Zempel include Max Planck Society & German Center for Neurodegenerative Diseases.

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Aβ Oligomers Cause Localized Ca2+ Elevation, Missorting of Endogenous Tau into Dendrites, Tau Phosphorylation, and Destruction of Microtubules and Spines

TL;DR: The A β-induced effects on microtubule and mitochondria depletion, Tau missorting, and loss of spines are prevented by taxol, indicating that Aβ-induced microtubules destabilization and corresponding traffic defects are key factors in incipient degeneration.
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Amyloid‐β oligomers induce synaptic damage via Tau‐dependent microtubule severing by TTLL6 and spastin

TL;DR: In neurons derived from Tau‐knockout mice, MTs and synapses are resistant to Aβ toxicity because TTLL6 mislocalization and MT polyglutamylation are prevented; hence no spastin recruitment and no MT breakdown occur, enabling faster recovery.
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Lost after translation: Missorting of Tau protein and consequences for Alzheimer disease

TL;DR: In Alzheimer disease and other tauopathies, Tau sorting mechanisms fail and Tau becomes missorted into the somatodendritic compartment, and the underlying mechanisms, and effects in disease are focused on.
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Novel diffusion barrier for axonal retention of Tau in neurons and its failure in neurodegeneration

TL;DR: A retrograde barrier in the axon initial segment (AIS) operating as cellular rectifier allows anterograde flow of axonal Tau but prevents retrograde flow back into soma and dendrites, which link the pathological hallmarks of Tau missorting and hyperphosphorylation in neurodegenerative diseases.
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Axodendritic sorting and pathological missorting of Tau are isoform-specific and determined by axon initial segment architecture

TL;DR: It is found that the Tau diffusion barrier (TDB), located within the axon initial segment (AIS), controls retrograde and anterograde traffic of Tau and that the axodendritic distribution of Tau depends on AIS integrity.