Back

The Human LRRK2-R1441G Mutation Drives Age-Dependent Oxidative Stress and Mitochondrial Dysfunction in Dopaminergic Neurons

Chen, Y.; Zhi, L.; Cui, S.; Wang, H.; Zeng, C.; Zhang, H.

2025-06-17 neuroscience
10.1101/2025.06.16.660029 bioRxiv
Show abstract

Mitochondrial dysfunction and oxidative stress are central to Parkinsons disease (PD) pathogenesis, particularly affecting substantia nigra pars compacta (SNc) dopamine (DA) neurons. Here, we investigate how the R1441G mutation in leucine-rich repeat kinase 2 (LRRK2), a key genetic contributor to familial and sporadic PD, impacts mitochondrial function in midbrain DA neurons. Using a BAC transgenic mouse model overexpressing human LRRK2-R1441G, we crossed these mice with TH-mito-roGFP mice, enabling mitochondria-targeted redox imaging in DA neurons. The two-photon imaging of acute brain slices from 3-, 6-, and 10-month-old mice revealed a progressive elevated oxidative stress in SNc DA neurons and their striatal projections, accompanied with reduced respiratory complex activity and decline in mitochondrial health. Spatial transcriptomics via GeoMx Digital Spatial Profiler identified molecular changes linked to dysregulated mitochondrial uncoupling protein function and calcium homeostasis. These findings demonstrate age-dependent mitochondrial dysfunction in LRRK2-mutant SNc DA neurons, highlighting calcium channels and uncoupling proteins as potential therapeutic targets to slow PD progression.

Matching journals

The top 7 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.