Parkinson's Disease Mechanisms and Treatments

This study prioritizes Parkinson’s Disease genes using transcriptomic data, identifying 29 peripheral monocyte and 44 prefrontal cortex gene associations, including novel and known genes like MAPT.

This study shows reduced beta rebound in Parkinson's disease patients during proprioceptive stimulation compared to healthy controls, suggesting impaired cortical processing of proprioceptive feedback independent of dopaminergic effects.

This study shows gut bacteria convert L-DOPA to dopamine, reducing its bioavailability and explaining variable dosing needs in Parkinson’s patients.

This paper uses deep neural networks on NMS-MRI to predict Parkinson’s disease with higher accuracy than traditional methods.

This study investigates whether Parkinson’s disease patients have deficits in updating sensory representations after eye movements, linking these deficits to dopaminergic system integrity.

The paper confirms the absence of the LRRK2 p.G2019S mutation in a larger Nigerian cohort of Parkinson's disease patients and controls, supporting its origin after human dispersal from sub-Saharan Africa.

The paper identifies Parkinson's risk variants in a SNCA enhancer by analyzing open chromatin in mouse dopamine neurons and validates their function in zebrafish and mice.

This study investigates whether β-synuclein overexpression via AAV can inhibit α-synuclein aggregation in a synucleinopathy model, but finds no delay in disease onset and reports specific β-synuclein aggregates in treated mice.

This study investigates how dopamine levels in Parkinson’s disease patients affect sensory attenuation during voluntary movements, finding a negative correlation with motor severity and a positive correlation with dopamine dose.

This study investigates how Parkinson’s disease and dopamine affect working memory by testing digit span tasks in patients and healthy controls with and without medication.

This study characterizes a fluorescent MPP+ mimic to investigate its cellular and mitochondrial uptake mechanisms and identifies a role for mitochondrial calcium homeostasis in its toxicity.

This study identifies a genetic variant at the TRIM11 locus associated with Progressive Supranuclear Palsy phenotype through GWAS and validates it in independent cohorts.

The paper reports the cryo-EM structure of alpha-synuclein fibrils, revealing key features relevant to disease mechanisms and therapeutic design.

The paper shows that Engrailed-1 protects dopaminergic neurons from degeneration by repressing LINE-1 expression, which is linked to oxidative stress-induced DNA damage.

The paper identifies genetic modifiers of LRRK2 G2019S-induced neurodegeneration in Drosophila using the DGRP, revealing 177 candidate genes and four significant modifiers affecting locomotor dysfunction.

This study shows that reducing Trim28 in adult mice is safe and lowers levels of alpha-synuclein and tau.

This paper develops a conditional human neural stem cell model to study alpha-synuclein effects on cell behavior and toxicity in Parkinson's disease.

This study examines the relationship between peripheral inflammation, measured by NLR, and striatal dopamine transporter binding in PD patients, finding significant correlations in tremor-dominant subtypes.

The paper uses single-cell RNA-seq to identify candidate genes for sporadic Parkinson’s disease by comparing DA neuron subpopulations and integrating with GWAS data.

This study identifies genes that protect C. elegans dopaminergic neurons from oxidative stress, showing that glit-1, tsp-17, the apoptosis pathway, and crt-1 are required to prevent 6-OHDA-induced neurodegeneration.

The paper identifies TTR-33 as a neuroprotective factor against 6-OHDA-induced dopaminergic neurodegeneration in C. elegans, showing its role in oxidative stress resistance and interaction with MAPK pathways.

This study finds that high baseline white matter hyperintensities (WMHs) in de novo Parkinson’s disease patients are linked to greater cognitive decline and cortical thinning compared to low WMHs or controls.

The paper shows that cortical thinning in early Parkinson’s Disease correlates with connectivity to subcortical disease reservoirs, suggesting disease spread along neural networks.

This study identifies a clinical-anatomical signature of Parkinson’s Disease using partial least squares and MRI, showing that atrophy patterns predict clinical progression.