Dem IPB wird erneut ein beispielhaftes Handeln im Sinne einer chancengleichheitsorientierten Personal- und Organisationspolitik bescheinigt. Das Institut erhält zum 6. Mal in Folge das TOTAL E-QUALITY…
Die Plant Science Student Conference (PSSC) wird seit 20 Jahren im jährlichen Wechsel von Studierenden der beiden Leibniz-Institute IPK und IPB organisiert. Im Interview erläutern Christina Wäsch…
Arndt, H.; Bachurski, M.; Yuanxiang, P.; Franke, K.; Wessjohann, L. A.; Kreutz, M. R.; Grochowska, K. M.;A screen of plant-based natural products revealed that quercetin prevents pyroglutamylated amyloid-β (Aβ3(pE)-42) uptake in astrocytes as well as resulting astrogliosis and synaptic dysfunctionMol. Neurobiol.623730–3745(2025)DOI: 10.1007/s12035-024-04509-6
Two connected histopathological hallmarks of Alzheimer’s disease (AD) are chronic neuroinflammation and synaptic dysfunction. The accumulation of the most prevalent posttranslationally modified form of Aβ1–42, pyroglutamylated amyloid-β (Aβ3(pE)-42) in astrocytes is directly linked to glial activation and the release of proinflammatory cytokines that in turn contribute to early synaptic dysfunction in AD. At present, the mechanisms of Aβ3(pE)-42 uptake to astrocytes are unknown and pharmacological interventions that interfere with this process are not available. Here we developed a simple screening assay to identify substances from a plant extract library that prevent astroglial Aβ3(pE)-42 uptake. We first show that this approach yields valid and reproducible results. Second, we show endocytosis of Aβ3(pE)-42 oligomers by astrocytes and that quercetin, a plant flavonol, is effective to specifically block astrocytic buildup of oligomeric Aβ3(pE)-42. Importantly, quercetin does not induce a general impairment of endocytosis. However, it efficiently protects against early synaptic dysfunction following exogenous Aβ3(pE)-42 application.