Parkinson's Disease Mechanisms and Treatments

The paper identifies complement and coagulation cascade pathways as significantly altered in two Parkinson's disease mouse models through proteome analysis.

This study shows that antisense oligonucleotides targeting alpha-synuclein reduce Lewy body pathology and improve cognitive and motor performance in a mouse model of synucleinopathy.

This study identifies altered mitochondrial and energy metabolism in PARK2 mutant human iPSC-derived dopaminergic neurons through metabolomic analysis.

The paper examines how loss of park7 activity affects IRE gene sets in zebrafish, suggesting iron dyshomeostasis and oxidative stress may differentially impact 5' and 3' UTR IREs in Parkinson's disease.

This study shows that motor cortical pyramidal neurons in Parkinsonism exhibit cell-type-specific decreases in intrinsic excitability due to impaired ion channel function.

This study investigates the effects of a DAT mutation linked to DTDS, showing impaired dopamine function and behavioral deficits in Drosophila, with potential therapeutic implications.

This study examines how inducing alpha-synuclein pathology in engineered human neural networks affects network criticality, revealing subtle changes in network function before overt symptoms appear.

The paper identifies genome-wide dysregulation of histone acetylation in Parkinson's disease brains, linking it to disease-related genes and altered gene expression.

This study identifies genetic modifiers of LRRK2 mutations in Parkinson's disease, finding a significant variant in CORO1C and a polygenic risk score effect on penetrance.

This study shows that baseline striatal dopamine transporter density inversely correlates with the rate of worsening neuropsychiatric symptoms in Parkinson's disease over four years.

The paper identifies VGLUT expression as a sex-dependent mediator of age-related dopamine neuron vulnerability in Parkinson's disease.

This study investigates sex-specific genetic factors in Parkinson's disease using GWAS but finds no significant genetic differences between male and female cases.

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

The paper shows that SERCA activity is reduced in DJ-1 mutant flies and human cells due to oxidative modification, and that activating SERCA can restore PD-related phenotypes.

The paper shows that experimental colitis increases alpha-synuclein accumulation in the gut and brain, linking intestinal inflammation to Parkinson's disease pathology.

This study identifies genetic associations with Parkinson disease motor subtypes using GWAS, finding novel variants and suggesting overlap with essential tremor genetics.

This study evaluates LIN28A variants in Parkinson's disease using genotyping and sequencing data, finding no strong evidence for a major causal role but suggesting further research in non-European populations is needed.

The paper investigates the degradation of DJ-1/PARK7 missense mutants in Parkinson's disease, showing that mitochondrial LonP1 protease mediates the degradation of some unstable mutants.

This study examines the genetic association between ANG variants and Parkinson's disease using large-scale genotype and whole genome sequencing data, finding no significant association.

This study shows that α-synuclein accumulation in presynaptic terminals causes synaptic dysfunction and progressive neurodegeneration in a Drosophila model, with similar findings in patient samples.

This study investigates how amyloid β affects future freezing of gait in Parkinson's Disease through white matter hyperintensities, independent of other factors.

The paper analyzes sncRNA-seq data from the PPMI cohort to identify miRNAs associated with Parkinson's disease progression and systemic inflammation.

This study shows that CSP reduces synuclein aggregates and restores dopamine release in a Parkinson's disease mouse model.

This study investigates how parkin's redox state and insolubility in human midbrain relate to oxidative stress and dopamine metabolism, showing that parkin's cysteine modifications affect H2O2 levels and neuroprotection.

This study identifies a Kv4 channelopathy in mouse vagal motoneurons caused by α-synuclein overexpression, leading to impaired gastrointestinal motility as a non-motor prodromal symptom of Parkinson's disease.

This study shows that LRRK2 G2019S kinase activity promotes NSF aggregation, which is toxic to neurons, and that autophagy can clear these aggregates and improve motor and cognitive function in a mouse model.

This study links cognitive dysfunction in Parkinson's disease to increased timing variability and reduced midfrontal ~4 Hz EEG activity during interval timing tasks.

This study shows that T cells reduce phosphorylated α-synuclein pathology in a mouse model of α-synucleinopathy.

This paper introduces a protease protection assay to distinguish internalized alpha-synuclein PFFs from surface-bound ones using TEV protease.