Vera I. Wiersma

Feb 14, 2024 | nature.com | Marian Hruska-Plochan |Vera I. Wiersma |Katharina M. Betz |Elena Tantardini |Florent Laferrière |Igor Delvendahl | +11 more

AbstractHuman cellular models of neurodegeneration require reproducibility and longevity, which is necessary for simulating age-dependent diseases. Such systems are particularly needed for TDP-43 proteinopathies1, which involve human-specific mechanisms2,3,4,5 that cannot be directly studied in animal models.

Jul 11, 2023 | embopress.org | Manuela Pérez-Berlanga |Vera I. Wiersma |Aurélie Zbinden |Laura De Vos

Loss of RNA binding or oligomerization differentially modulate the subcellular localization of TDP-43 inclusions Decline of the cellular proteostasis capacity with age contributes to protein misfolding in neurodegenerative diseases (Jayaraj et al, 2020), often resulting in the accumulation of ubiquitinated inclusions in affected tissues, including TDP-43 proteinopathies (Arai et al, 2006; Neumann et al, 2006).