Polo-like kinase inhibition leads to neuroprotection of neurons bearing alpha-synuclein Lewy body-like inclusions .

α-synuclein (αSyn) and S129 phosphorylated αSyn (pSyn) define synucleinopathies like Parkinson's disease (PD). Targeting S129 αSyn kinases, like the Polo-like kinase (PLK) family, could provide a therapeutic strategy to limit degeneration of cells bearing aggregated αSyn inclusions. Using longitudinal multiphoton imaging in mouse cortex after αSyn inclusion induction, we find an increase in cell survival of inclusion-bearing neurons after PLK inhibition.

No impact of COVID-19 at delivery on maternal mortality or infant adverse birth outcomes in Botswana during the Omicron era.

SARS-CoV-2 infection during pregnancy was associated with maternal mortality and adverse birth outcomes in the pre-Omicron era, including a stillbirth rate of 5.6% in Botswana. We re-evaluated these outcomes in the Tsepamo Study during the Omicron era.

Parameter estimation in a whole-brain network model of epilepsy: Comparison of parallel global optimization solvers.

The Virtual Epileptic Patient (VEP) refers to a computer-based representation of a patient with epilepsy that combines personalized anatomical data with dynamical models of abnormal brain activities. It is capable of generating spatio-temporal seizure patterns that resemble those recorded with invasive methods such as stereoelectro EEG data, allowing for the evaluation of clinical hypotheses before planning surgery. This study highlights the effectiveness of calibrating VEP models using a global optimization approach.

Alpha-synuclein regulates the repair of genomic DNA double-strand breaks in a DNA-PK-dependent manner.

α-synuclein (αSyn) is a presynaptic and nuclear protein that aggregates in important neurodegenerative diseases such as Parkinson's Disease (PD), Parkinson's Disease Dementia (PDD) and Lewy Body Dementia (LBD). Our past work suggests that nuclear αSyn may regulate forms of DNA double-strand break (DSB) repair in HAP1 cells after DNA damage induction with the chemotherapeutic agent bleomycin. Here, we report that genetic deletion of αSyn specifically impairs the non-homologous end-joining (NHEJ) pathway of DSB repair using an extrachromosomal plasmid-based repair assay in HAP1 cells.