Parkinson's Disease Mechanisms and Treatments

This study uses C. elegans to show that α-synuclein pre-formed fibrils induce prion-like aggregation and neurotoxicity, with protective effects from targeting heparan sulfate proteoglycan biosynthesis.

The paper investigates how CDK5 phosphorylates cPLA2 in Parkinson's Disease, leading to neuroinflammation and identifies potential therapeutic targets.

This study examines the age-dependent effects of rotenone exposure on mice, showing increased neurological susceptibility in younger mice with seizures and cellular changes in the hippocampus.

This study investigates how metabolic demand influences selective cell death in Parkinson's Disease by simulating neural cells with altered biophysical properties.

This study identifies risk genes in Parkinson's disease using microarray data analysis with WGCNA and DEGs methods, finding genes associated with motor and non-motor symptoms.

This study shows that neuronal hemoglobin overexpression in mice leads to dopaminergic neuron loss, cognitive deficits, and cleavage of α-synuclein.

This study uses a novel microfluidic system to investigate how alpha-synuclein aggregates spread between neurons, finding that synaptic connectivity does not significantly affect transfer efficiency.

The paper develops a PLA method to specifically detect endogenous pS129 α-synuclein in tissue with low background and high specificity.

This study identifies Auxilin mutations as a cause of Parkinson's disease by showing they impair clathrin-mediated trafficking at the Golgi and synapse, leading to neuropathological lesions.

This study investigates the anti-dyskinetic effects of vitamin D3 in a Parkinsonian mouse model, finding it reduces abnormal involuntary movements and modulates oxidative stress, inflammation, and apoptosis.

The paper reports sex-specific DNA methylation changes in Parkinson's disease-associated genes in cortical neurons from post-mortem parietal cortex samples.

This study identifies five RBD risk loci through genome-wide association and finds differential expression of SNCA-AS1 and SCARB2 in brain regions.

This study shows that glycation worsens Parkinson's-like symptoms in mice by enhancing glutamatergic signaling and causing dopaminergic neuron loss.

This study shows that LRRK2 kinase activity causes centrosomal cohesion deficits through phosphorylated Rab10 and RILPL1 at centriolar subdistal appendages.

The paper proposes a multi-view workflow for integrating imaging and genetic data in Parkinson's Disease to identify potential genetic biomarkers.

This study shows that intracerebral Ifenprodil improves motor function and protects dopamine neurons in 6-OHDA-injured rats by enhancing autophagy and reducing microglial activation.

This study uses patient-specific midbrain organoids with SNCA triplication to show synaptic decline precedes dopaminergic neuron loss in Parkinson's disease.

This study identifies VCP as a suppressor of proteopathic seeding and shows that VCP dysfunction increases seeding of multiple aggregates, contributing to neurodegeneration.

This study compares α-synuclein fibril structures from Parkinson's disease and Multiple System Atrophy patients, showing differences in their quaternary arrangement and effects on oligodendroglial cells.

Three fibril polymorphs, amplified from Parkinson's and multiple system atrophy brain homogenate by PMCA, adopt folds unlike any published alpha-synuclein arrangement; their disease relevance is untested.

This study investigates the risk mechanism of rs356182, a PD risk SNP near SNCA, by generating CRISPR-Cas9 lesions in LUHMES cells and observing effects on neuronal differentiation and axonogenesis.

This study investigates neuronal activity in LRRK2-G2019S mutant neurons and finds increased spontaneous calcium transients and shorter inter-spike intervals.

The paper identifies ten distinct midbrain dopaminergic neuron populations in Parkinson's disease, highlighting an AGTR1-expressing subtype vulnerable to degeneration and associated with PD risk genes.

This study shows that Fyn kinase inhibition with AZD0530 improves recognition memory and reduces depressive-like behavior in a Parkinson's disease model, though it does not reduce microglial activation.

This study shows DOPAL promotes αSynuclein accumulation and impairs proteostasis in neuronal projections, contributing to Parkinson's disease progression.

This study uses machine learning to predict Parkinson's disease onset and subtype from germline variants, achieving ROC scores of 0.77 and 0.61.

This study identifies DNA methylation and hydroxymethylation changes in dopaminergic neurons overexpressing alpha-synuclein variants, linking them to altered gene expression in PD-related pathways.

This study examines how polygenic risk scores influence the penetrance of monogenic Parkinson's disease variants and family history in Parkinson's disease risk.

The paper demonstrates that neuronal NOX2 contributes to oxidative stress, α-synuclein pathology, and LRRK2 activation in Parkinson's disease and shows that NOX2 inhibitors can prevent these effects in a rat model.

This study identifies a mechanism by which α-synuclein is loaded into exosomes via Ndfip1, leading to Parkinson's-like pathology in mice.