Gan Lab
@LiGanLab
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We've moved to Bluesky! Please follow us there! https://t.co/pbbp33G3QU
New York
Joined July 2019
Two separate studies from Gitler & Fratta labs reveal nuclear loss of TDP-43 disrupts RNA processing by altering alternative 3′ end cleavage & polyadenylation. They uncover new molecular signatures & shed light on TDP-43 pathology https://t.co/DqZ6NMtMUA
https://t.co/McwUOV23Ib
nature.com
Nature Neuroscience - Zeng et al. show that TDP-43, known for repressing cryptic exon usage in frontotemporal dementia/amyotrophic lateral sclerosis, also controls alternative polyadenylation,...
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Check out this @NatureNeuro piece written by @Yale_INP graduate @suzhou_yang and @YaleNeuro @KavliAtYale Postdoc Fellow @zhenlei_ , highlighting recent works by Gitler, @FrattaLab, and La Spada labs on the impact of TDP-43 pathology on mRNA 3' ends in ALS
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Fascinating study from the Mao & Jiang lab: four amino acid residues unique to naked mole-rat cGAS, but absent in humans, are critical for efficient DNA repair, delaying aging and expanding life span.
science.org
Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that...
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Mao, Han & Dawson reveal air pollutant PM2.5 triggers αSyn misfolding, forming a pathogenic strain(PM-PFF) that drives Lewy body dementia. This work illuminates the link between air pollution & neurodegenerative disease, offering insights for public health
science.org
Evidence links air pollution to dementia, yet its role in Lewy body dementia (LBD) remains unclear. In this work, we showed in a cohort of 56.5 million individuals across the United States that fine...
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Collaborative work from Zhang Cai & Peng labs identifies glia-neuron protein co-expression subnetwork as central driver of AD from multiscale genetic & proteomic analyses. AHNAK emerges as key astrocytic driver whose downregulation reduces pTau & Aβ levels
cell.com
Multiscale proteomic network modeling of Alzheimer's disease integrates large-scale proteomic and genetic data from vulnerable brain regions and reveals key driver proteins such as AHNAK within a...
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Wu lab discovers early neuronal hyperactivity in TDP-43 induces rod-shaped microglia, which attenuates cortical hyperactivity, suggesting a neuroprotective role. Coincidentally, TREM2 signaling also promotes rod-shaped MG & neuroprotection.
cell.com
While microglial activation is a hallmark in neurodegeneration, the specific role of microglia in disease-related cortical excitability remains unknown. Xie et al. reveal that rod-shaped microglia...
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Yu & Sun identify TFEB as a molecular link between neurons & oligodendrocytes (OL) in myelination. Neuronal signals trap TFEB in OL's cytoplasm, keeping TFEB from entering nucleus & repressing cholesterol biosynthesis genes, which causes hypomyelination https://t.co/q34tVNERO2
cell.com
Zhang et al. identify TFEB as a molecular link that connects extrinsic neuronal cues to intrinsic oligodendrocyte transcriptional programs. TFEB directly binds to and represses numerous cholesterol...
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Interesting study from Xu, Zhang & Mo labs: oxidized mtDNA can transform into Z-DNA & activate ZBP1-RIPK1-dependent inflammation in AD microglia. This highlights ZBP1-RIPK1 as a key regulatory axis of neuroinflammation
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🏆🏆🏆 CONGRATULATIONS to the winner of the PBL Assay Science Best Speaker Award Sarah Naguib @naguib_sarah! Title: Elucidating the neuroprotective mechanisms of human microglial replacement therapy in FTD and PD Thank you PBL Assay Science for sponsoring the award
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The Kolachama Lab is tackling the PET scan bottleneck in Alzheimer’s diagnosis with an AI model that predicts amyloid-β & tau status from 12,185 patients across 7 cohorts, offering a scalable alternative for pre-screening & guiding PET imaging.
nature.com
Nature Communications - A flexible AI framework integrates multimodal neurology work-up data to estimate amyloid and tau burden, supporting scalable biomarker stratification for Alzheimer’s...
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Exciting finding led by Dr. Bruce Yankner: Endogenous lithium is essential for brain health and its deficiency contributes to the onset and progression of Alzheimer’s disease, by activating GSK3β—leading to impaired Aβ clearance and synapse loss 🔗
nature.com
Nature - Lithium has an essential role in the brain and is deficient early in Alzheimer’s disease, which can be recapitulated in mice and treated with a novel lithium salt that restores the...
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