Nora Bengoa‐Vergniory

This paper creates a humanised GBA-L444P mouse model to study GBA1 mutations in Parkinson's, finding gain-of-function effects on dopamine release and loss-of-function effects on alpha-synuclein pathology.

This paper introduces ASA-PD, an imaging method to detect and map α-synuclein oligomers in Parkinson's disease brain tissue, revealing a specific subpopulation of nanoscale oligomers as an early hallmark of the disease.

This study shows gabapentinoids enhance dopamine release in a Parkinson's mouse model and improve movement deficits by modulating calcium and GABAergic signaling.

This study shows that the GBA-N370S mutation causes early hyperexcitability in striatal neurons by reducing sodium and potassium currents, which can be mitigated by aging or PKA antagonism.

The paper shows adult mouse SCN astrocytes respond to glucocorticoids through GR activation, influencing circadian rhythms and highlighting astrocytic roles in time-keeping.

This study shows that reducing tau in human neurons decreases A beta toxicity, supporting the role of tau in Alzheimer's disease mechanisms.

This study shows LAG3 is not expressed in human and mouse neurons and does not worsen α-synuclein pathology in vitro or in vivo.

This study develops a transgenic mouse model expressing human alpha-synuclein in noradrenergic neurons, revealing LC pathology and non-motor PD features.

The paper investigates the role of astrocytic GABA transporters in regulating dopamine release in the striatum and shows their downregulation in early parkinsonism.