Markus Glatzel

The paper identifies astrocyte-driven small vessel disease as an early, amyloid-independent feature of PSEN1 E280A familial Alzheimer's disease through proteomic and transcriptomic analyses.

This study identifies Aβ42-carrying extracellular vesicles in plasma as biomarkers associated with neurodegeneration and neuroinflammation in Alzheimer's disease.

This study shows that extracellular vesicles from cortical neurons alter spontaneous activity in recipient neurons by increasing postsynaptic potential amplitude.

This paper introduces a tunable fiber-optic dispersive wave generator for deep-tissue two-photon imaging in mouse brains, achieving high-resolution imaging at depths over 450 micrometers.

This paper introduces a three-color ultrafast fiber laser platform for multiplexed two-photon imaging, validated in mouse tissue to visualize multiple cellular structures.

The paper identifies altered CD4 T-cell immune profiles in NSCLC patients with oligo-metastatic brain disease compared to poly-metastatic disease and healthy controls.

This paper demonstrates that non-enzymatic methods can isolate brain-derived extracellular vesicles without compromising protein integrity, achieving high yield and purity.

This study identifies ADAM10-mediated shedding of human PrP at Y226 and shows sPrP associates with misfolded protein aggregates in neurodegenerative diseases.

This study examines the effects of SARS-CoV-2 infection on astrocytes and microglial cells in the frontal cortex of COVID-19 patients compared to controls, finding microgliosis, astrogliosis, and loss of AQP4 polarity.

This study shows that katanin, a microtubule-severing complex, is located at dendritic spines and regulates microtubule polymerization and synaptic plasticity through activity-dependent processes.

The paper shows that ligands binding to PrPC induce its proteolytic release, which has neuroprotective effects, and identifies mechanisms and exceptions in this process.

This study characterizes brain-derived extracellular vesicles (sEVs) in mice under normal and post-stroke conditions, showing increased PrP and PrP-C1 content and altered cellular uptake.