Group of passionate scientists unraveling the mysteries of neurodegeneration at Weill Cornell Medicine 🧠 | Tackling Alzheimer’s, FTD, PD & related diseases 🧬 | Focused on tau, innate immunity, & targeted therapeutics using iPSC & transcriptomics🔬
Gan Lab
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Our new JCI review discusses the cGAS-STING pathway's evolution & molecular roles beyond inflammation & highlights how activation affects glial states, neuronal homeostasis, & BBB integrity, yielding new therapeutic paths in neurodegenerative disease www.jci.org/articles/vie...
In our latest preprint, we show microglia protect against levodopa-induced dyskinesia (LID): microglia-derived sTREM2 acts on TrkB, boosts BDNF-TrkB signaling, and points to plasticity as a potential Parkinson’s/LID therapy biorxiv.org/content/10.64898/2026.05.06.723382v1
PanNDA leverages deep proteomics of 2,279 human brain samples in AD, LBD, FTD-TDP-43, PSP, VD, & PD to reveal shared disease mechanisms, spotlighting GPNMB (microglial/lysosomal activation) & NPTX2 (synaptic regulation). Paper: www.cell.com/cell/fulltex.... Data: penglab.shinyapps.io/pannda.
Gan lab takes on Central Park zoo! Groups ideated, wrote and shot 2-4min short videos about intriguing CP zoo lore last Friday. Awesome time storytelling and collaborating with everyone!
Lu et al. profiled >10,000 plasma & CSF samples to uncover how APOE2 & APOE4 confer divergent AD risk. APOE2 protects by sustaining homeostatic & anti-inflammatory signatures before Aβ accumulation, whereas APOE4 proteomic changes respond after pathology www.nature.com/articles/s43...
The 13th Annual Appel Symposium on Mar 24 spotlighted the interconnectedness of neurodegenerative diseases. Drs. Sreeganga Chandra (Yale), Eddie Lee (UPenn), & Anna Orr (Appel) gave keynote presentations, preceded by over two dozen trainee posters from Appel & collaborating labs
New in Nature: de Faria et al. show focal white matter lesions trigger remote microglial response to demyelinated neurons in grey matter, which is required for remyelination. Deplete grey matter microglia→repair failures→chronic grey matter inflammation
doi.org/10.1038/s415...
Paquet lab addresses iPSC limitation: new line with endogenous P301L/S320F 4R tau develops age-related tauopathy phenotypes stem cells typically fail to model. Platform shows pathological tau aggregation for more precise tauopathy research & drug screening
www.science.org/doi/10.1126/...
Excited to share our spotlight article in Cell Stem Cell on CAR-A astrocyte therapy for Alzheimer’s disease, an innovative approach for in vivo amyloid clearance. We discuss both the promise and the challenges ahead. 🧠
www.sciencedirect.com/science/arti...
MAPT p.R406W disrupts autophagy–lysosome pathway, impairing Tau degradation. Mutant neurons accumulate Tau/pTau in lysosomes, impairing motility, autophagosome fusion, & clearance. Autophagy enhancement lowers Tau & restores degradation but doesn't rescue trafficking www.nature.com/articles/s41...
A pan-neurodegeneration atlas built from multilayer, deep proteomics of 2,279 brain
samples across 6 major diseases integrates whole proteome, detergent-insoluble proteome,
and posttranslational modif...
A transient grey matter microgliosis is required for remyelination, the failure of which results in a chronic neuroinflammatory state seen in neurodegenerative disorders.
Apolipoprotein E (APOE) is the strongest genetic influence in Alzheimer’s disease (AD). Compared to the most frequent allele, ε3, the ε4 allele increases AD risk, and the ε2 allele is protective. Here...
In a recent study in Science, Chen et al. engineer astrocytes with anti-amyloid chimeric antigen receptors (CARs) to enable sustained, antigen-directe…
Researchers show that a disease-causing Tau mutation disrupts the autophagy-lysosome pathway in human neurons, leading to Tau accumulation, and that enhancing autophagy can partially restore protein c...
