@Rothstein_Lab

Dr. Jeffrey Rothstein is a professor of neurology and neuroscience @HopkinsMedicine and is the founding director of @packardcenter. (trainee run)

 Baltimore, MD
rothsteinlab.org
Joined April 2023
  • Tweets2.6K
  • Following393
  • Followers1.4K
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Rothstein Lab retweeted
Suleyman Can Akerman@CanAkermanSep 3
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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Rothstein Lab retweeted
Suleyman Can Akerman@CanAkermanAug 7
Multi-omics of C9orf72 spinal cord organoids reveal convergent molecular signatures and targets researchsquare.com/article/r…

Multi-omics of C9orf72 spinal cord organoids reveal convergent molecular signatures and targets

Background: amyotrophic lateral sclerosis is the most common adult-onset motor neuron disease, characterised by the progressive degeneration of upper and lower motor neurons in the brain and spinal...

researchsquare.com
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Rothstein Lab retweeted
ShorterLab@ShorterLabAug 6
α-Synuclein blocks endoplasmic reticulum co-translational protein translocation early in Parkinson’s disease: nature.com/articles/s41467-0…

α-Synuclein blocks endoplasmic reticulum co-translational protein translocation early in Parkinso...

Nature Communications - Proteomic and transcriptomic profiling on hiPSC-derived midbrain dopaminergic neurons with pathological α-synuclein burden reveals defective Sec61A interactions and...

nature.com
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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/10.64898…

ESCRT Machinery Dysfunction in Motor Neurone Disease: TSG101, CHMP2B, and VPS4a Differentially...

Motor Neurone Disease (MND) is characterised by progressive degeneration of upper and lower motor neurons, accompanied by cytoplasmic mislocalisation and hyperphosphorylation of TDP-43 — hallmarks...

biorxiv.org
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Mitochondria directly interact with the nuclear pore complex nature.com/articles/s41586-0…

Mitochondria directly interact with the nuclear pore complex

Nature - Mitochondria interact directly with the nuclear pore complex via VDAC1–RANBP2 binding to sustain nuclear ATP levels.

nature.com
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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/nene20…). Thank you to the organizers for putting together such a nice program, and grateful for all the feedback and discussion!
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Rothstein Lab retweeted
Charlotte Fare@charlotte_fareJun 13
TDP-43 self-assembly is regulated by its disordered NLS-region biorxiv.org/content/10.64898…

TDP-43 self-assembly is regulated by its disordered NLS-region

Cytosolic inclusions of the RNA-binding protein TDP-43 are a pathological hallmark of several neurodegenerative diseases, such as amyotrophic lateral sclerosis and frontotemporal dementia. Cellular...

biorxiv.org
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Rothstein Lab retweeted
ShorterLab@ShorterLabApr 23
Astrocytes connect specific brain regions through plastic networks: nature.com/articles/s41586-0…

Astrocytes connect specific brain regions through plastic networks

Nature - Communication between distant brain regions is mediated by plastic networks of gap junction-coupled astrocytes.

nature.com
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Rothstein Lab retweeted
ShorterLab@ShorterLabApr 23
Rab27b: A Modulator of Lysosomal Function and Alpha-Synuclein Clearance in Parkinson's Disease jneurosci.org/content/46/16/…

Rab27b: A Modulator of Lysosomal Function and Alpha-Synuclein Clearance in Parkinson's Disease

Lysosomes are often referred to as the cell's recycling center, serving as the terminal degradative compartments of the endolysosomal and autophagic systems, through which cellular waste is broken...

jneurosci.org
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TMEM106B C-terminal fragments drive nucleocytoplasmic transport failure and TDP-43 mislocalization in the aging human brain biorxiv.org/content/10.64898…
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Rothstein Lab retweeted
Suleyman Can Akerman@CanAkermanFeb 9
Novel extracellular vesicle release pathway facilitated by toxic superoxide dismutase 1 oligomers sciencedirect.com/science/ar…
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Lysosomal escape and TMEM106B fibrillar core determine TDP-43 seeding outcomes biorxiv.org/content/10.64898…

Lysosomal escape and TMEM106B fibrillar core determine TDP-43 seeding outcomes

Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) shows striking clinical and neuropathological heterogeneity, yet a systematic analysis of subtype-specific features and inter-pat...

biorxiv.org
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Rothstein Lab retweeted
MND Research
@mndresearch12 Dec 2025
Last week, we held the 36th #alsmndsymp in San Diego. The essence of the International Symposium is to bring the global community together and drive #MND #ALS research forward. 🌍 Read more about this year's symposium on our blog ⬇️ mndresearch.blog/2025/12/12/…
A lecture theater packed with people listening to a talk.

ALT A lecture theater packed with people listening to a talk.

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Large-scale drug screening in iPSC-derived motor neurons from sporadic ALS patients identifies a potential combinatorial therapy nature.com/articles/s41593-0…

Large-scale drug screening in iPSC-derived motor neurons from sporadic ALS patients identifies a...

Nature Neuroscience - In this study, the authors generated iPSC lines from more than 100 sporadic ALS cases, which recapitulated key disease phenotypes and enabled large-scale drug screening,...

nature.com
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Rothstein Lab retweeted
ShorterLab@ShorterLab21 Nov 2025
A rare genetic variant confers resistance to neurodegeneration across multiple neurological disorders by augmenting selective autophagy: Neuron cell.com/neuron/fulltext/S08…

A rare genetic variant confers resistance to neurodegeneration across multiple neurological...

In Croce et al. the discovery of a rare SNP in the Venezuelan HD kindreds that is associated with a delayed age of onset of up to 23 years reveals how preventing aberrant protein accumulation is...

cell.com
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We’re hiring! Two postdoc positions are open in the Translational Neuroproteomics lab at Mayo Clinic Florida, focusing on tau and TDP-43 proteinopathies and neurodegeneration. mayo.edu/research/labs/trans… Apply here: 1) fa-euwp-saasfaprod1.fa.ocs.o… 2) fa-euwp-saasfaprod1.fa.ocs.o… Please share!

Overview - Translational Neuroproteomics - Translational Neuroproteomics Laboratory

Dr. Rossoll's Translational Neuroproteomics Laboratory at Mayo Clinic focuses on new treatments for motor neuron and neurodegenerative disease.

mayo.edu
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Rothstein Lab retweeted
ShorterLab@ShorterLab15 Nov 2025
A human forebrain organoid model phenocopies dysregulated RNA and protein homeostasis in ALS/FTD-associated TDP-43 proteinopathies biorxiv.org/content/10.1101/…

A human forebrain organoid model phenocopies dysregulated RNA and protein homeostasis in ALS/FTD-...

Background TAR DNA-binding protein 43 ( TDP-43) proteinopathy is a central hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet current experimental models fail to...

biorxiv.org
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PolyGR-containing aggregates link with pathology and clinical features of Alzheimer’s disease link.springer.com/article/10…

PolyGR-containing aggregates link with pathology and clinical features of Alzheimer’s disease

Acta Neuropathologica - Alzheimer’s disease is the most common form of dementia; however, its molecular mechanisms are not fully understood. We recently identified...

link.springer.com
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Differences and overlaps in TDP-43 pathology of ‘pure’ LATE-NC compared to LATE-NC coexisting with Alzheimer’s disease link.springer.com/article/10…
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C9orf72 ALS‐causing mutations lead to mislocalization and aggregation of nucleoporin Nup107 into stress granules febs.onlinelibrary.wiley.com…

FEBS Press

Mutations in the C9orf72 gene represent the most common genetic cause of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease. Using patient-derived neurons and C. elegans models,...

febs.onlinelibrary.wiley.com
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