Michael G. Schlossmacher

This study shows ASC-Syn assemblies enhance NLRP3 inflammasome activation in microglia and co-localize with Lewy body pathology in human brain tissue.

This study shows that Lrrk2 p.G2019S mutant mice exhibit increased phosphorylated α-synuclein and tau in the brain after influenza A infection, suggesting a link between LRRK2 mutations and neurodegeneration.

This study shows optogenetic stimulation of nigral astrocytes reduces motor deficits and dopamine neuron loss in a 6-OHDA model of Parkinson's disease.

This study shows that Lrrk2 and Snca gene variants do not affect encephalitis severity in newborn mice infected with reovirus T3D via direct brain inoculation, unlike intranasal infection.

This paper presents a method to generate olfactory organoids from adult mice to study environmental interactions with the olfactory epithelium and disease processes.

This study shows that reducing CDK14 genetically or pharmacologically decreases alpha-synuclein pathology and improves symptoms in Parkinson's disease models.

This study maps the expression and dosage of alpha-Synuclein across cell types in the mouse brain and periphery, identifying high and low expressing cell types and their potential role in Parkinson's disease.

BATL is a Bayesian classifier for targeted lipidomics that annotates LC-ESI-MS/MS peaks with high accuracy using eight features, achieving over 95% correct identification in SRM datasets.

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 shows that mGluR5 pharmacology and Aβ oligomer-induced signaling differ between male and female Alzheimer's mice, with implications for sex-tailored treatments.

The paper shows that α-synuclein fibrils activate LRRK2 kinase in monocyte-derived macrophages, linking LRRK2 mutations to pro-inflammatory responses in Parkinson's disease.

This study shows that parkin reduces oxidative stress in mammalian brains by mediating H2O2 reduction and glutathione regeneration, but its absence leads to increased oxidative stress despite compensatory mechanisms.

This study identifies oxidative modifications of parkin in adult human brain that confer neuroprotection by reducing H2O2, conjugating dopamine radicals, and forming neuromelanin.