Rothstein Lab @Rothstein_Lab
Dr. Jeffrey Rothstein is a professor of neurology and neuroscience @HopkinsMedicine and is the founding director of @packardcenter. (trainee run) rothsteinlab.org Baltimore, MD Joined April 2023-
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Rothstein Lab retweeted
Great to be part of #ALSNexus26 last week! I presented our work on modulating extracellular vesicles to inhibit dipeptide repeat propagation in C9-ALS, both in the Emerging Science session and as a poster. Great discussions across the ALS community. #ALS
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TDP-43-related cryptic splicing reflects pathological heterogeneity in amyotrophic lateral sclerosis link.springer.com/article/10.118…
TTBK1 Inhibitors Modulate TDP-43 Pathology and Rescue Cognitive Deficits in a Mouse Model of TDP-43 Proteinopathy pubs.acs.org/jmcmar/article…
EPHA2/CD44-directed trafficking enhances endosomal leakiness and antisense therapy delivery rupress.org/jcb/article/22…
Rothstein Lab retweeted
Multi-omics of C9orf72 spinal cord organoids reveal convergent molecular signatures and targets researchsquare.com/article/rs-100…
Impaired Motor Function in a Zebrafish Stathmin-2 Knockout Model onlinelibrary.wiley.com/doi/10.1002/dn…
Rothstein Lab retweeted
α-Synuclein blocks endoplasmic reticulum co-translational protein translocation early in Parkinson’s disease: nature.com/articles/s4146…
Astrocyte dysfunction distinguishes monozygotic twin C9orf72 expansion carriers discordant for amyotrophic lateral sclerosis biorxiv.org/content/10.648…
Deep axonal proteomics of human iPSC-derived neurons by microfluidic separation and DIA-MS biorxiv.org/content/10.648…
Schwann Cell–Specific TDP-43 Rescue Improves Peripheral Nerve Myelin Pathology Without Altering Motor Behaviour in a Mouse Model of ALS biorxiv.org/content/10.648…
Rothstein Lab retweeted
Intersting preprint: blocking VPS4a could keep TDP-43 out of exosomes without stopping exosome production. That would suggest that one might be able to block the neuron-to-neuron spread of pathology without shutting down normal vesicle trafficking. biorxiv.org/content/10.648…
Therapeutic targeting of the conserved region within the low-complexity domain of TDP-43 is neuroprotective and extends survival in amyotrophic lateral sclerosis mice nature.com/articles/s4358…
Striatal neuron dysfunction in C9ORF72-FTD/ALS is driven by AIS and potassium channel dysregulation sciencedirect.com/science/articl…
STMN2 protein depletion via translation deficits and stress granules in amyotrophic lateral sclerosis academic.oup.com/brain/advance-…
An open-label Phase 2a study of fasudil in amyotrophic lateral sclerosis: safety and exploratory endpoints tandfonline.com/doi/10.1080/21…
Rothstein Lab retweeted
Mitochondria directly interact with the nuclear pore complex nature.com/articles/s4158…
Rothstein Lab retweeted
Excited to have shared our work on Nucleoporin210 in a tauopathy model at the Northeast Nuclear Envelope 2026 meeting at Yale (sites.google.com/view/nene2026/…). Thank you to the organizers for putting together such a nice program, and grateful for all the feedback and discussion!
Rothstein Lab retweeted
TDP-43 self-assembly is regulated by its disordered NLS-region biorxiv.org/content/10.648…
Downregulation of miRNAs Accompanies Increased HERV-K (HML-2) Expression in Amyotrophic Lateral Sclerosis link.springer.com/article/10.100…
Development and characterization of 3D spinal cord organoids to advance the study of amyotrophic lateral sclerosis link.springer.com/article/10.118…
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