Changjoon Justin Lee

This paper describes a method to convert reactive astrocytes into functional motor neurons with high efficiency and specificity using TRANsCre-DIONE, leading to improved motor recovery in spinal cord injury.

This study identifies the AXL-ICD/SIRT2 axis as a mechanism by which amyloid-β impairs astrocytic autophagy and exacerbates neuroinflammation in Alzheimer's disease.

This study investigates how dopamine modulates striatopallidal synapses in different GPe subregions, revealing region-specific presynaptic and postsynaptic inhibition mechanisms.

The paper shows that astrocytic Best1 mediates a switch in tonic inhibition in cerebellar granule cells during adolescence, enhancing motor coordination through network-level changes.

This study identifies the astrocytic MAOB-GABA axis as a brake on spinal cord injury repair and shows that the inhibitor KDS2010 promotes recovery in animal models and has a safe profile in humans.

This study identifies H2O2-induced astrocytic collagen production as a mechanism causing neuronal death in ischemic stroke, with potential therapeutic targets identified.

This study identifies nalfurafine and nalmefene as agents that cause long-lasting KOR inactivation, potentially offering new therapeutic approaches for stress-related disorders.

This study shows that astrocytic volume transients mediated by TREK-1 and TRPA1 channels are essential for synaptic plasticity and spatial memory.

Acupuncture alleviates both motor and non-motor symptoms in Parkinson's disease by activating two distinct MCH projections.

This paper identifies hemoglobin as a peroxidase with therapeutic potential for oxidative stress-related diseases and presents KDS12025 as a drug candidate that enhances its activity.

SUBTLE maps animal behavior from 3D action skeletons using an unsupervised framework, achieving superior performance in capturing behavioral repertoires and identifying inter-group differences through temporal representation.

This paper develops a fast, sensitive genetically encoded H2O2 sensor (oROS-G) and demonstrates its use in monitoring H2O2 dynamics in various cell types and models.

This study identifies GABRA5-positive neurons in the lateral hypothalamic area that regulate obesity through astrocytic GABA release, showing that inhibiting astrocytic GABA reduces weight gain.

This study investigates the role of PAT/SAT1 in MAO-B-dependent GABA synthesis in astrocytes, showing that PAT/SAT1 gene silencing reduces GABA synthesis and tonic inhibition.

The paper demonstrates that PET/CT imaging with 11C-acetate and 18F-FDG can visualize reactive astrocyte-mediated neuronal hypometabolism in Alzheimer's disease.

The paper identifies ALDH1A1 and SIRT2 as enzymes in the astrocytic putrescine-to-GABA metabolic pathway and suggests they are potential therapeutic targets for Alzheimer's Disease.

This study identifies TMEM87A as a novel Golgi-resident cation channel, GolpHCat, which regulates pH homeostasis and is essential for brain function and memory.

This study identifies TMEM43 as a pH-sensing cation channel that modulates gap junction networks in the hippocampus, preventing neuronal hyperexcitability and supporting memory retrieval.

This study shows that dopamine-modified hyaluronic acid (DA-HA) has dopamine-like functionality with reduced autoxidation and toxicity, making it a potential therapeutic alternative to L-DOPA for Parkinson's disease.

This study shows that astrocytic urea cycle detoxifies Aβ-derived ammonia but impairs memory in Alzheimer's disease, suggesting ODC1 inhibition as a potential therapeutic strategy.

The paper identifies Bergmann glia in the cerebellum as mediators of noxious information processing and their role in modulating pain-related behaviors.

This study uses CRISPR/Cas9 to delete A53T-SNCA in a rat model of Parkinson's disease, showing reduced -synuclein levels and improved motor symptoms.

This study shows astrocytes regulate NMDAR tone through Best1-mediated glutamate and D-serine release, which is essential for cognitive flexibility and memory repotentiation during reversal learning.

The paper uses intravital imaging to study cellular changes after cerebral microinfarction in mice, finding that astrocyte reactivity leads to glial scar formation.

This study identifies TMEM43 mutations as a cause of autosomal dominant auditory neuropathy spectrum disorder by showing their interaction with Connexin-mediated channels in cochlear glia-like supporting cells.

This study shows that both vesicular and non-vesicular gliotransmission from astrocytes are necessary for synaptic plasticity and working memory, with impaired release causing memory deficits.