Xiaobo Mao

This study introduces an ultra-rare AKAP11 protein-truncating variant in mice, showing it causes anxiety- and depression-like behaviors and disrupts PKA signaling.

This paper develops PMO-based RNA-degrading chimeras that target SNCA mRNA to reduce α-synuclein levels and prevent pathological aggregation in vitro and in vivo.

This study identifies microglial Lag3 as a key receptor linking extracellular α-synuclein PFF recognition to neurotoxic astrocyte conversion and dopaminergic neurodegeneration.

The paper shows a copper-containing nanozyme worsens alpha-synucleinopathy by increasing nitrosative stress, while a copper-free version reduces pathology in neurodegenerative models.

This paper introduces a chemiluminescence probe, ADLumin-1, that enables both generic and precise detection of misfolded proteins in neurodegenerative disease models.

This study shows neuronal LAG3 is essential for α-synuclein propagation and neurodegeneration in Parkinson's disease, suggesting LAG3 as a therapeutic target.

The paper identifies distinct α-synuclein strains associated with cognitive decline in Parkinson's disease and shows AI-based analysis of these strains improves clinical stratification.

This paper identifies NOD2/RIPK2 signaling as a key driver of neuroinflammation in Parkinson's disease, showing that pathological α-synuclein activates this pathway in microglia, leading to neurodegeneration and that targeting NOD2 or RIPK2 protects dopamine neurons.

This study identifies Lag3 as a neuronal receptor for Tau preformed fibrils, essential for their uptake, propagation, and transmission in Tauopathies.

This paper shows edaravone protects mRNA-induced motor neurons from neurotoxicity by activating the GDNF/RET signaling pathway and can replace neurotrophic factors for neuron survival.

The paper identifies Aplp1 and its complex with Lag3 as facilitators of pathologic alpha-synuclein transmission and toxicity, showing that disrupting this complex prevents neurodegeneration.