Michael X. Henderson

The paper quantifies Lewy pathology burden in the putamen across Lewy body diseases and finds it accumulates in excitatory synapses before synaptic degeneration.

The paper analyzes longitudinal histopathology data to show that α-synuclein pathology follows rise-and-fall dynamics, revealing a vulnerability axis linked to energy metabolism and monoaminergic neurons.

This study shows chronic H. pylori infection causes brain inflammation and dopaminergic neuron loss through inflammation, independent of α-synuclein pathology, and eradication reduces these effects.

This study shows that tau filament seeding capacity depends on both core structure and phosphorylation in the fuzzy coat, with phospho-mimetic residues restoring activity in modified tau.

This study shows that pathological α-synuclein can cause granulovacuolar degeneration independently of tau, using a mouse model of α-synucleinopathy.

The paper identifies group II p21-activated kinases as regulators of α-synucleinopathy by linking network vulnerability analysis to gene expression and pharmacological interventions.

The paper identifies that Tet2 loss promotes ciliogenesis and reduces α-synuclein pathology in Parkinson's disease models.

The paper uses spatial transcriptomics to identify specific cortical neurons vulnerable to Lewy pathology in PD and discovers a conserved molecular dysfunction signature in both mice and humans.

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.

This study shows that LRRK2 kinase inhibition reverses tau pathology progression in mice with the G2019S mutation but not in wildtype mice.

This study identifies up-regulation of human endogenous retrovirus (HERV) transcripts in Parkinson's disease (PD) across multiple tissues and blood, linking TE activation to PD pathogenesis and potential treatment monitoring.

The paper examines the relationship between glucocerebrosidase activity, lipid levels, and protein pathologies in Parkinson's disease and dementia with Lewy bodies.

This study investigates how alpha-synuclein aggregation in the basolateral amygdala affects glutamatergic transmission, finding that it selectively disrupts cortico-BLA synapses.

This paper introduces a deep learning model for automated microglia morphology analysis, validated across mouse disease models and available on a commercial platform.

This study shows tau pathology spreads along anatomical brain connections and a LRRK2 mutation alters its directionality in mice.