Joel Blanchard

The paper identifies microglial states associated with Parkinson's disease genetic risk and Lewy body pathology using single-cell profiling and integrates data with AMP PD.

The paper introduces ExRPath and 15ExMPath techniques to expand human brain tissue for nanostructure analysis, revealing amyloid nanoclusters associated with SARS-CoV-2 in COVID-19 patients.

The paper shows ATP13A2 loss of function disrupts polyamine metabolism, leading to SAM depletion and epigenetic astrocyte toxicity, which contributes to Parkinson's disease.

SingleBrain integrates snRNA-seq and genotype data to map cis-eQTLs across brain cell types, identifying novel disease-associated genes and causal variants.

The paper constructs a 3D human brain model integrating multiple cell types to study Alzheimer's Disease mechanisms linked to APOE4.

The paper identifies Wnt signaling defects and GSK3b overactivity as regulators of lipid accumulation in APOE4 oligodendrocytes, showing that inhibiting GSK3b reduces lipid droplets and improves myelination.

This study identifies APOE4-driven pericyte-to-myofibroblast transition in cerebrovascular disease, leading to fibrosis and amyloid deposition, and shows TGF-β inhibition can reverse these effects.

This study shows that ATP10B loss causes dopaminergic neuron death and Parkinsonian symptoms in rats and human stem cell models.

The paper compares dopaminergic neurons from siblings with Gaucher disease to investigate genetic factors contributing to Parkinsonism.

The paper develops GEM-SCOPe, a modular fluorescent tool to study lysosomal and mitochondrial dysfunction in Parkinson's disease, identifying disease-related changes in organelle behavior.

This study develops a human brain tissue model (miBrain) to show that APOE4 astrocytes with cholesterol dysregulation promote α-synuclein pathology through endolysosomal dysfunction.

This study shows that impaired lysosomal proteolysis in astrocytes leads to proteostasis failure in midbrain neurons in an early-onset PD model.