Herman Li

Dual kinase inhibition provides early clues to restoration of neuroimmune homeostasis in an AAV-haSyn model of Parkinsons disease

This study shows that dual inhibition of MLK3 and LRRK2 with URMC-099 reduces PD pathology and motor deficits in an AAV-haSyn rat model.

Dynamics of Neutrophilia at the Neurovascular Unit Arising from Repeated Pulmonary Inflammation

This study investigates how repeated pulmonary inflammation leads to neutrophil dynamics at the neurovascular unit, showing increased neutrophilia and microglial activation in the brain.

Sez6L2 autoimmunity induces cerebellar ataxia in mice

This study shows that Sez6L2 autoimmunity in mice causes cerebellar ataxia, with antibodies and T cells targeting Sez6L2 leading to mobility impairments and brain inflammation.

Noradrenergic signaling controls Alzheimer's disease pathology via activation of microglial β2 adrenergic receptors

This study shows that microglial β2 adrenergic receptors modulate Alzheimer's disease pathology by reducing inflammation and amyloid pathology in mouse models.

URMC-099 Prophylaxis Prevents Hippocampal Vascular Vulnerability and Synaptic Damage in an Orthopedic Model of Delirium Superimposed on Dementia

The paper investigates the effects of URMC-099 in preventing vascular and synaptic damage in a mouse model of delirium superimposed on dementia.

A Quantum Dot Biomimetic for SARS-CoV-2 to Interrogate Dysregulation of the Neurovascular Unit Relevant to Brain Inflammation

This study uses a SARS-CoV-2 biomimetic to investigate how BBB dysregulation may lead to neuroinflammation without direct viral infection.

The Sez6 family inhibits complement at the level of the C3 convertase.

This study shows that Sez6 family members inhibit C3 convertase activity in both classical and alternative complement pathways.

Complement-dependent synapse loss and microgliosis in a mouse model of multiple sclerosis

This study investigates complement-dependent synapse loss and microgliosis in EAE mice, finding that C3 knockout reduces synapse loss and microglial activation.