🔬 Molecular Neurodegeneration research group at Tel Aviv University, Israel

Joined February 2019
14 Photos and videos
Perlson lab retweeted
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive weakness due to degeneration of upper motor neurons in the brain and lower motor neurons in the brainstem and spinal cord. Learn more in this Review: ja.ma/3Q8S0jq
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Perlson lab retweeted
Mecca et al. investigate the role of muscle stem cells in SMA and show that their depletion disrupts neuromuscular junctions and leads to motor neuron loss in the spinal cord. They conclude that muscle stem cells represent potential therapeutic targets. shorturl.at/vIwEU
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Perlson lab retweeted
Annexin A7 enhances TIA1 axonal trafficking to counteract pathological aggregation in neurons embopress.org/doi/full/10.10…

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Perlson lab retweeted
Annexin A7 enhances TIA1 axonal trafficking to counteract pathological aggregation in neurons | The EMBO Journal embopress.org/doi/full/10.10…

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Perlson lab retweeted
23 Oct 2025
O'Brien et al. demonstrate a link between ALS and extreme exercise in males which is potentially mediated via failed mTOR signalling at the neuromuscular junction. tinyurl.com/cajta7y3; tinyurl.com/ymd5c6h4
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Perlson lab retweeted
Drs. Yi Zeng, Aaron Gitler, and colleagues show that loss of TDP-43 from neuronal nuclei of human brain and disease-causing mutations in TDP-43 are associated with widespread changes in alternative polyadenylation. 🧠 @StanfordMed @NatureNeuro | go.nature.com/473g5Oe
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Perlson lab retweeted
22 Oct 2025
Retrotransposons unplugged: Rewiring the nervous system and wreaking havoc: Neuron cell.com/neuron/fulltext/S08…

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Our cover art suggestion. Firefighters spraying mir126 balloons to douse the flames- toxic TDP-43 aggregates that damage axons and neuromuscular junction in ALS. Illustration by Maayan Visuals. nature.com/articles/s41593-0…
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Thrilled to share our new work in Nature Neuroscience! Together with amazing collaborators and led by Ariel Ionescu, we discovered that muscle-derived miR-126 controls local axonal TDP-43 synthesis and protects neuromuscular junctions in ALS. nature.com/articles/s41593-0…
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By uncovering a new mechanism that drives ALS progression and identifies a potential therapeutic target, we hope this work opens up new avenues for intervention. Grateful to my brilliant team and collaborators for making this possible.
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This reveals a novel muscle-to-motor neuron communication axis, where loss of miR-126 triggers TDP-43 accumulation, NMJ disruption, and motor decline. Restoring miR-126 demonstrated neuroprotective effects in both mouse and human ALS models.
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