Melissa McAlonis-Downes

发表

Reduced C9ORF72 function exacerbates gain of toxicity from ALS/FTD-causing repeat expansion in C9orf72

L. Petrucelli, Huaxi Xu, A. L. La Spada, 2020, Nature Neuroscience.

Misfolded SOD1 Associated with Motor Neuron Mitochondria Alters Mitochondrial Shape and Distribution Prior to Clinical Onset

Sameer B. Shah, J. Julien, D. Cleveland, 2011, PloS one.

Overriding FUS autoregulation in mice triggers gain-of-toxic 1 dysfunctions in RNA metabolism and autophagy-lysosome axis 2 3

Debbie, Shuying, Gene W. Yeo, 2022 .

ALS-linked TDP-43 mutations produce aberrant RNA splicing and adult-onset motor neuron disease without aggregation or loss of nuclear TDP-43

Gene W. Yeo, C. Shaw, L. Tessarollo, 2013, Proceedings of the National Academy of Sciences.

Progressive spinal axonal degeneration and slowness in ALS2‐deficient mice

Timothy A. Miller, D. Cleveland, K. Yamanaka, 2006, Annals of neurology.

Macrophage Migration Inh ibitory Factor as a Chaperone Inhibiting Accumulation of Misfolded SOD 1

Huilin Zhou, B. Kaspar, D. Cleveland, 2015 .

C1q induction and global complement pathway activation do not contribute to ALS toxicity in mutant SOD1 mice

C. Pozniak, D. Cleveland, C. Lobsiger, 2013, Proceedings of the National Academy of Sciences.

Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

C. Heyser, L. Petrucelli, C. Shaw, 2016, Neuron.

Misfolded SOD1 is not a primary component of sporadic ALS

D. Pizzo, D. Cleveland, J. Ravits, 2017, Acta Neuropathologica.

Comprehensive preclinical evaluation of human-derived anti-poly-GA antibodies in cellular and animal models of C9ORF72 disease

L. Petrucelli, R. Nitsch, C. Hock, 2022, bioRxiv.

Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration

Gene W. Yeo, S. Vandenberg, Xiang-Dong Fu, 2013, Proceedings of the National Academy of Sciences.

Stathmin-2 loss leads to neurofilament-dependent axonal collapse driving motor and sensory denervation

C. Lutz, F. Rigo, P. Jafar-Nejad, 2022, bioRxiv.

Enhancing Mitochondrial Calcium Buffering Capacity Reduces Aggregation of Misfolded SOD1 and Motor Neuron Cell Death without Extending Survival in Mouse Models of Inherited Amyotrophic Lateral Sclerosis

D. Cleveland, Joo Seok Han, S. Da Cruz, 2013, The Journal of Neuroscience.

An endogenous peptide marker differentiates SOD1 stability and facilitates pharmacodynamic monitoring in SOD1 amyotrophic lateral sclerosis.

M. Benatar, J. Wuu, F. Rigo, 2019, JCI insight.

ALS/FTD-Linked Mutation in FUS Suppresses Intra-axonal Protein Synthesis and Drives Disease Without Nuclear Loss-of-Function of FUS

C. Shaw, Xiang-Dong Fu, G. Hicks, 2018, Neuron.

Antisense oligonucleotide therapy for neurodegenerative disease.

B. Monia, C. Bennett, D. Cleveland, 2006, The Journal of clinical investigation.

Spinal subpial delivery of AAV9 enables widespread gene silencing and blocks motoneuron degeneration in ALS

Shang Gao, Shawn P. Driscoll, Samuel L. Pfaff, 2019, Nature Medicine.

Mutant SOD1 in cell types other than motor neurons and oligodendrocytes accelerates onset of disease in ALS mice

L. Goldstein, O. Mikse, D. Cleveland, 2008, Proceedings of the National Academy of Sciences.

Translational profiling identifies a cascade of damage initiated in motor neurons and spreading to glia in mutant SOD1-mediated ALS

L. Ferraiuolo, B. Kaspar, Kevin Drenner, 2015, Proceedings of the National Academy of Sciences.

Macrophage Migration Inhibitory Factor as a Chaperone Inhibiting Accumulation of Misfolded SOD1

Huilin Zhou, B. Kaspar, D. Cleveland, 2015, Neuron.

Schwann cells expressing dismutase active mutant SOD1 unexpectedly slow disease progression in ALS mice

D. Cleveland, K. Yamanaka, C. Lobsiger, 2009, Proceedings of the National Academy of Sciences.

Therapeutically viable generation of neurons with antisense oligonucleotide suppression of PTB

A. Muotri, T. Hnasko, F. Rigo, 2021, Nature Neuroscience.

Wild-type FUS corrects ALS-like disease induced by cytoplasmic mutant FUS through autoregulation

D. Cleveland, S. Megat, C. Lagier-Tourenne, 2020, bioRxiv.

Mutant TDP-43 within motor neurons drives disease onset but not progression in amyotrophic lateral sclerosis

D. Pizzo, Kevin Drenner, D. Cleveland, 2017, Acta Neuropathologica.

Elevated PGC-1α activity sustains mitochondrial biogenesis and muscle function without extending survival in a mouse model of inherited ALS.

B. Spiegelman, C. Lillo, David S. Williams, 2012, Cell metabolism.

Gain of Toxicity from ALS / F TD-Linked Repeat Expansions in C 9 ORF 72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs Highlights

C. Heyser, L. Petrucelli, C. Shaw, 2016 .

ALS/FTD-Linked Mutation in FUS Suppresses Intra-axonal Protein Synthesis and Drives Disease Without Nuclear Loss-of-Function of FUS

C. Shaw, Xiang-Dong Fu, G. Hicks, 2020, Neuron.

Overriding FUS autoregulation in mice triggers gain-of-toxic dysfunctions in RNA metabolism and autophagy-lysosome axis

Gene W. Yeo, C. Shaw, G. Tucker-Kellogg, 2019, eLife.

Antisense oligonucleotide therapy for neurodegenerative disease.

B. Monia, C. Bennett, D. Cleveland, 2006, The Journal of clinical investigation.

Schwann cells expressing dismutase active mutant SOD1 unexpectedly slow disease progression in ALS mice

D. Cleveland, K. Yamanaka, C. Lobsiger, 2009, Proceedings of the National Academy of Sciences.

Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

C. Heyser, L. Petrucelli, F. Rigo, 2016, Neuron.

Supplemental Information Gain of Toxicity from Als/ftd-linked Repeat Expansions in C9orf72 Is Alleviated by Antisense Oligonucleotides Targeting Ggggcc-containing Rnas

C. Heyser, Kevin Drenner, Jie Jiang, 2022 .

Frontotemporal dementia-like disease progression elicited by seeded aggregation and spread of FUS

J. Shorter, Sonia Vazquez-Sanchez, Melissa McAlonis-Downes, 2024, Molecular neurodegeneration.