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John Ravits

As seen in: Nature, JAMA (The Journal of the American Medical Association), JAMA Network, JAMA: Journal of the American Medical Association, Cell Press
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Articles by John Ravits

Antisense Oligonucleotide Tofersen Distribution in the Central Nervous System of SOD1 -ALS Autopsy Tissue Donors

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By Amanda J. Guise, Shanu Roemer, Michael Monine, Nicole Harris, Dan Bartlett, Eric M. David, Shanqin Xu, Andrew King, Robert Bowser, Vladislav A. Korobeynikov, John Ravits, Pamela Shaw, Toby Ferguson, Stephanie Fradette, Danielle Graham, Eric Sorenson, Björn Oskarsson, R. Ross Reichard, Dennis W. Dickson, Sabrina Paganoni, Suma Babu, Derek Oakley, Matthew P. Frosch, Timothy Miller, Robert C. Bucelli, Richard Perrin, Cindy Ly, Edward D Plowey, Monica Thanawala Sellon, Luke Jandreski, Sohail Malek, Steve Garafalo, Ivan Nestorov, Margaret D. Ireland, J. Robin Highley
| JAMA Network Verified
Antisense Oligonucleotide Tofersen Distribution in the Central Nervous System of SOD1-ALS Autopsy Tissue Donors Key Points Question What is the biodistribution of tofersen and its impact on SOD1 levels in human central nervous system tissues?
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An emergent disease-associated motor neuron state precedes cell death in ALS

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By Olivia Gautier, Jacob Blum, Thao Nguyen Verified, Thảo Nguyen, Shaolong Cao, Sandy Klemm, Mai Yamakawa, Dann Huh, Jessica Hurt, Nasa Sinnott-Armstrong, Yi Zeng, Juliane Bombosch, Chang Liu, Lisa Encarnacion, Kevin A. Guttenplan, Derek Chen, Arwa Kathiria, Luke Zhao, Stephen Moore, Don W. Cleveland, John Ravits, Jessica Rexach, William J. Greenleaf, Aaron D. Gitler, Alex Meng, Kailee Ong
| Cell Press Verified
Keywords ALS neurodegeneration spinal cord motor neuron selective vulnerability snRNA-seq snATAC-seq spatial transcriptomics cell states microglial activation Introduction Amyotrophic lateral sclerosis (ALS) is a progressive disorder distinguished by degeneration of motor neurons in the brain and spinal cord. Motor neuron loss impairs mobility, dexterity, speech, and swallowing and ultimately causes fatal paralysis. ALS is a cruelly rapid disease.
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An emergent disease-associated motor neuron state precedes cell death in ALS

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By Olivia Gautier, Jacob Blum, Thao Nguyen Verified, Thảo Nguyen, Shaolong Cao, Sandy Klemm, Mai Yamakawa, Dann Huh, Jessica Hurt, Nasa Sinnott-Armstrong, Yi Zeng, Juliane Bombosch, Chang Liu, Lisa Encarnacion, Kevin A. Guttenplan, Derek Chen, Arwa Kathiria, Luke Zhao, Stephen Moore, Alex Meng, Kailee Ong, Don W. Cleveland, John Ravits, Jessica Rexach, William J. Greenleaf, Aaron D. Gitler
| Cell Press Verified
Introduction Amyotrophic lateral sclerosis (ALS) is a progressive disorder distinguished by degeneration of motor neurons in the brain and spinal cord. Motor neuron loss impairs mobility, dexterity, speech, and swallowing and ultimately causes fatal paralysis. ALS is a cruelly rapid disease. Most patients survive just 3 to 5 years after diagnosis.1 Effective therapies depend on defining the cellular and molecular drivers of motor neuron degeneration.
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Amyotrophic Lateral Sclerosis : A Review

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By John Ravits
| JAMA: Journal of the American Medical Association Verified
Abstract Importance 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. It affects approximately 25 000 individuals in the United States.
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Somatic mosaicism in ALS and FTD identifies focal mutations associated with widespread degeneration

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By Zinan Zhou, Junho Kim, August Yue Huang, Matthew Nolan, Junseok Park, Ryan Doan, Taehwan Shin, Michael Miller, Boxun Zhao, Jinhyeong Kim, Katherine Morillo, Rebecca C. Yeh, Connor J. Kenny, Jennifer Neil, Takuya Ohkubo, John Ravits, Olaf Ansorge, Lyle W. Ostrow, Clotilde Lagier-Tourenne, Eunjung Lee, Christopher Walsh, Mingyun Bae, Brian Chhouk, Chao-Zong Lee
| Nature Verified
Abstract Although mutations in many genes cause familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), most cases are sporadic (sALS and sFTD) with unclear etiology. Here we tested whether somatic mutations contribute to sALS and sFTD by deep targeted sequencing of 88 neurodegeneration-related genes in postmortem brain and spinal cord samples from 399 sporadic cases and 144 controls.
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Author Correction: Autoimmune response to C9orf72 protein in amyotrophic lateral sclerosis

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By Tanner Michaelis, Emil Johansson, April Frazier, Gregory Williams, James Berry, Merit E. Cudkowicz, Namita Goyal, Christina N. Fournier, Allison Snyder, Justin Kwan, Elizabeth Phillips, Simon A. Mallal, John Ravits, Karen S. Marder, John Sidney, David Sulzer, Alessandro Sette, Cecilia S. Lindestam Arlehamn, Jody Crook
| Nature Verified
Correction to: Nature https://doi.org/10.1038/s41586-025-09588-6 Published online 1 October 2025 In the version of the article initially published, Gregory P. Williams (Center for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, USA) was missing from the author list and contributions and has now been added to the HTML and PDF versions of the article.
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An α2-Na/K ATPase/α-adducin complex in astrocytes triggers non-cell autonomous neurodegeneration

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By Gilbert Gallardo, Jessica Barowski, John Ravits, Teepu Siddique
| Nature Verified
Abstract Perturbations of astrocytes trigger neurodegeneration in several diseases, but the glial cell–intrinsic mechanisms that induce neurodegeneration remain poorly understood. We found that a protein complex of α2-Na/K ATPase and α-adducin was enriched in astrocytes expressing mutant superoxide dismutase 1 (SOD1), which causes familial amyotrophic lateral sclerosis (ALS).
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