Kelvin C. Luk

This study shows that synucleinopathy triggers complement activation and dysregulation before neurodegeneration in a rat model and human Parkinson's disease tissue.

NERINE tests gene network hypotheses with rare variant associations, identifying a subnetwork linked to Parkinson's disease.

This study compares how different BBB models affect immune cell trafficking in PD, showing that model architecture significantly influences results.

The paper shows that synucleinopathy in SLD glutamatergic neurons causes RBD and Parkinson's-like deficits in mice.

This study evaluates dapansutrile, an NLRP3 inhibitor, in preclinical models of Parkinson's disease and multiple system atrophy, showing improved motor function, reduced neurodegeneration, and transcriptomic changes in microglia.

This paper develops a mouse model of Parkinson's disease by overexpressing α-synuclein and demonstrates neuroprotection with PD180970.

This study shows that systemic XPro1595, a TNF inhibitor, does not protect against -Syn-induced Parkinson's-like pathology in rats, despite being effective in other neurodegeneration models.

This paper develops an iPSC platform to rapidly generate alpha-synuclein inclusions and investigates their formation, subtypes, and molecular interactions.

The paper identifies plasma α-synuclein conformations that distinguish Parkinson's disease from dementia with Lewy bodies and predict cognitive decline in PD.

This study introduces a G51D mutation in the rat Snca gene, leading to synaptic mislocalization of α-synuclein and increased susceptibility to Lewy-like pathology.

This study shows that developmental exposure to dieldrin worsens dopamine-related deficits in mice with synucleinopathy, suggesting environmental factors contribute to Parkinson's disease progression.

This study examines how reduced Ciita levels affect immune responses in a rat model of Parkinson's disease, finding increased TNF levels and altered MHCII expression in immune cells.

The paper shows that PKB/AKT activation protects dopamine neurons from ER stress and -syn aggregation via Cathepsins B and D, suggesting a potential gene therapy approach for Parkinson's disease.

This study shows LAG3 is not expressed in human and mouse neurons and does not worsen α-synuclein pathology in vitro or in vivo.

This study shows that activating the GDNF/RET signaling pathway prevents Lewy Body pathology in dopamine neurons by blocking α-synuclein aggregation.

This study shows that α-Synuclein seeding in the olfactory bulb leads to altered odor-evoked neural activity in the olfactory system.

This paper develops a mouse model expressing aSyn-GFP under native regulatory elements, showing it mirrors endogenous aSyn expression and pathology.

This study shows that developmental dieldrin exposure increases male-specific motor deficits and dopamine handling issues in a synucleinopathy model, without affecting nigral neuron loss.

This study shows that PAR promotes α-synuclein aggregation and interacts with phosphorylated α-synuclein in Parkinson's disease samples.

The paper identifies potent small molecules that inhibit toxic alpha-synuclein oligomers and reduce cell death in SH-SY5Y cells using a FRET-based biosensor platform.

The paper shows that α-synuclein aggregates disrupt pacemaking in vulnerable nigrostriatal dopamine neurons via K-ATP channels, contributing to Parkinson's disease pathogenesis.

This paper demonstrates that antisense oligonucleotides targeting SNCA reduce alpha-synuclein production, prevent pathology, and show translational potential in non-human primates.