Parkinson's Disease Mechanisms and Treatments

This study identifies Mitoxantrone hydrochloride as a drug that targets APP and LRRK2 to improve neurodegeneration in Parkinson's disease models.

This study shows astrocytes process and propagate α-synuclein aggregates via lysosomal protease Cathepsin D, promoting Lewy neurite-like aggregation in neurons.

The paper identifies shared and sex-specific lipidomic changes in brain and plasma of Parkinson's disease models and patients, showing peripheral lipid signatures reflect CNS pathology.

This study investigates the cytoprotective effects of TMD nanoflowers on immune cells exposed to α-synuclein fibrils, finding MoSe2 NFs more effective in mitigating toxicity than MoS2 NFs.

This study maps the comorbid landscape of Parkinson's disease and Crohn's disease through a multi-omics approach, revealing shared genetic and transcriptional mechanisms along the gut-blood-brain axis.

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.

The paper evaluates polygenic risk scores for Parkinson's disease in a South African cohort, finding modest predictive performance and no ancestry-specific risk variants.

This study shows that MoS2 and MoSe2 nanoflowers reduce alpha-synuclein toxicity in neurons and astrocytes, improve mitochondrial function, and extend lifespan in C. elegans.

This study uses Boolean modeling on PD cohorts to show sex-specific miRNA dysregulation affects mitochondrial biogenesis, mitophagy, and autophagy in Parkinson's disease.

This study evaluates PHP.eB AAVs for reducing alpha-synuclein burden in a mouse model of alpha-synucleinopathies, showing reduced pathology and motor deficits.

This study uses ancestral sequence reconstruction to show that synuclein aggregation evolved progressively, with fibril formation emerging in an ancestral node and being suppressed in beta-synuclein.

The paper identifies two dimethoxyphenyl piperazine analogs that inhibit alpha-synuclein fibril growth in vitro and from Lewy Body Disease brain tissue.

This study identifies genetic variants associated with REM sleep behavior disorder in Parkinson's disease and explores genetic correlations with neuropsychiatric traits.

This study shows NLX-112 protects against MPTP-induced dopaminergic neuron loss in mice by reducing microgliosis, increasing GDNF, and improving locomotor activity.

This study shows that increasing mitochondrial NAD+ regeneration via MitoLbNOX does not rescue dopaminergic neuron dysfunction caused by complex I impairment in Parkinson's disease mice.

This study investigates how infection and pesticide exposure lead to α-Synuclein Ser129 phosphorylation through c-Abl kinase activation and identifies potential therapeutic targets.

This study investigates the association between COMT genetic variants and Parkinson's disease risk across diverse ancestries but finds no significant enrichment of COMT risk alleles in PD patients after multiple testing correction.

This study shows that stimulating the A13 region in Parkinson's mouse models improves locomotor function and reduces bradykinesia by restoring motor function through neural remodeling.

The paper develops an assay to compare protein levels and toxicity of alpha-synuclein variants, finding that the S129A mutant does not affect acute expression or toxicity.

This study shows that transmitted alpha-synuclein extracellular vesicles reduce retrograde axonal transport in recipient neurons, with effects dependent on endogenous alpha-synuclein interaction.

This study identifies secondary nucleation of α-Synuclein as the key mechanism driving mitochondrial dysfunction and Lewy body formation in Parkinson's 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 mild brain injury increases dopaminergic neurodegeneration and Lewy body pathology in mice, and that reducing T cell infiltration improves outcomes.

The paper uses super-resolution microscopy and SIMOA to analyze alpha-synuclein aggregates in Parkinson's disease brain samples and mouse models, finding larger aggregates in PD samples and differences based on extraction methods.

The paper identifies differentially expressed genes in Parkinson's disease brain tissues, highlighting SYT1 as a significantly downregulated gene associated with calcium signaling and neurotransmitter release.

This study shows that glycated alpha-synuclein assemblies cause distinct Parkinson's disease pathology in mice, including earlier onset of motor symptoms and increased neuroinflammation.

This paper develops a method to label alpha synuclein fibrils with fluorophores for tracking their structure and function in cells.

The paper investigates compensatory mechanisms in dopamine signaling during nigrostriatal neuron loss in a rat Parkinson model, finding that dopamine levels are preserved in the substantia nigra despite significant TH loss.

This paper identifies six PD subgroups based on cell-type-specific genetic networks and links NRG6 to reduced myelin integrity in oligodendrocytes.