Wenzhen Duan

This study shows that depletion of border-associated macrophages in HD mice impairs CSF flow and increases extranuclear mutant huntingtin aggregation.

This study shows that restoring aquaporin-4 in a Huntington disease mouse model improves glymphatic function and reduces disease-related molecular and motor phenotypes.

The paper introduces a computer vision framework to analyze fine motor behaviors in HD mice, identifying disease-specific motor signatures and a scoring system to assess therapeutic effects.

This study shows that vascular smooth muscle cell loss, not amyloidosis or neuroinflammation, causes cerebrovascular reactivity impairment in Alzheimer's disease.

The paper identifies microbleeds as a specific marker of amyloid-related vascular injury in 5xFAD mice, distinct from small-vessel disease.

The paper screens a kinase inhibitor library in HD iPSC-derived neurons to identify PKC alpha and beta1 inhibition as neuroprotective against mutant huntingtin toxicity.

This study characterizes the progression of the zQ175DN mouse model of Huntington disease, identifying early biomarkers like brain volume loss and plasma NfL elevation.

The paper identifies cell type-specific transcriptomic changes in 5XFAD mice that link BBB dysfunction and metabolic dysregulation to early AD pathogenesis.

This study uses quantitative susceptibility mapping to distinguish microgliosis and tau deposition in a mouse model of tauopathy by analyzing paramagnetic and diamagnetic susceptibility components.

This study shows that senolytic therapy with D+Q preserves BBB integrity and improves cognitive function in a tauopathy mouse model.

This study uses MRI and fluorescence imaging to show impaired glymphatic function in a mouse model of Huntington disease, suggesting it as a potential biomarker and therapeutic target.

This study develops a CRISPR-Cas13d system targeting CAG-expanded HTT RNA in HD models, reducing mutant mRNA and reversing disease phenotypes without significant off-target effects.

This paper describes the creation of a novel HD mouse model, BAC226Q, which accurately recapitulates age-dependent and progressive HD-like phenotypes.

This study shows that HTT silencing in premanifest HD mice delays disease onset and slows progression, using CBVa as a noninvasive biomarker.