Parkinson's Disease Mechanisms and Treatments

This study shows phospholipid bilayers catalyze α-synuclein aggregation from monomers, with efficiency depending on membrane composition and leading to dissociable aggregates.

The paper introduces a new parameter, VS, to detect bradykinesia in Parkinson's disease patients using the BRAIN tap test and validates its reliability across different hardware platforms.

This study develops a new Parkinson's disease mouse model showing that reducing α-synuclein aggregates rescues dopamine neuron dysfunction and death.

The paper correlates peripheral mitochondrial function with clinical severity in idiopathic Parkinson’s disease, finding stronger correlations with non-dopaminergic signs and reversible mitochondrial defects under metabolic stress.

This study connects Parkinson’s disease heritability to cell-type-specific gene regulation, finding enrichment in lysosomal genes in astrocytic and microglial subtypes rather than specific cell types or brain regions.

This paper identifies differentially expressed microRNAs in Parkinson’s disease through meta-analyses of multiple datasets, finding significant associations in brain and blood samples.

This study conducts a GWAS to identify genetic determinants of Parkinson's disease age of onset, finding associations with SNCA, TMEM175, and GBA, and highlighting alpha-synuclein's role in disease onset.

This study estimates the heritability of dementia with Lewy bodies (DLB) and finds it to be higher than previous estimates, with low variance explained by polygenic risk scores from Parkinson's or Alzheimer's disease.

The paper classifies Parkin variants into functional groups based on their impact on mitophagy and stability, revealing potential therapeutic targets for Parkinson’s disease.

This study shows that LRRK2 modifies α-syn aggregation and spread in both mouse and human models, suggesting potential therapeutic targets for Parkinson's disease.

This study shows that loss of one Engrailed1 allele in mice increases α-synuclein aggregation after PFF injection, suggesting a role for En1 in PD pathology.

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.