Robert H. Brown

Robert H. Brown, P. Andersen, E. Pioro, 2003, Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases.

Amyotrophic lateral sclerosis: pathogenesis.

W. Robberecht, R. Brown, R. H. Brown, 2000, Seminars in neurology.

Three novel mutations and two variants in the gene for Cu/Zn superoxide dismutase in familial amyotrophic lateral sclerosis

H. Horvitz, Robert H. Brown, R. Orrell, 1996, Neuromuscular Disorders.

An update on superoxide dismutase 1 in familial amyotrophic lateral sclerosis

Robert H. Brown, M. Cudkowicz, Robert H. Brown, 1996, Journal of the Neurological Sciences.

Amyotrophic Lateral Sclerosis.

Robert H. Brown, A. Al-Chalabi, Robert H. Brown, 2017, The New England journal of medicine.

Chapter 87 – Amyotrophic Lateral Sclerosis

Robert H. Brown, J. Sreedharan, Robert H. Brown, 2015 .

Neurodegenerative Diseases: The genetics of amyotrophic lateral sclerosis

Robert H. Brown, A. Al-Chalabi, Robert H. Brown, 2005 .

Identification of new mutations in the Cu/Zn superoxide dismutase gene of patients with familial amyotrophic lateral sclerosis.

V. Meininger, G. Rouleau, A. Pramatarova, 1995, American journal of human genetics.

Linkage of recessive familial amyotrophic lateral sclerosis to chromosome 2q33–q35

J. Haines, M. Pericak-Vance, Robert H. Brown, 1994, Nature Genetics.

An intersubunit disulfide bond prevents in vitro aggregation of a superoxide dismutase-1 mutant linked to familial amytrophic lateral sclerosis.

Robert H. Brown, P. Lansbury, T. Walz, 2004, Biochemistry.

Modulation of actin polymerization affects nucleocytoplasmic transport in multiple forms of amyotrophic lateral sclerosis

Eric W. Danielson, Robert H. Brown, J. Landers, 2018, Nature Communications.

Decoding ALS: from genes to mechanism

Robert H. Brown, J. Taylor, D. Cleveland, 2016, Nature.

dSarm/Sarm1 Is Required for Activation of an Injury-Induced Axon Death Pathway

Mary A. Logan, Robert H. Brown, S. Züchner, 2012, Science.

Excessive release of inorganic polyphosphate by ALS/FTD astrocytes causes non-cell-autonomous toxicity to motoneurons

Robert H. Brown, D. A. Bosco, F. González-Nilo, 2022, Neuron.

Adeno‐associated virus–delivered artificial microRNA extends survival and delays paralysis in an amyotrophic lateral sclerosis mouse model

Robert H. Brown, C. Mueller, M. ElMallah, 2016, Annals of neurology.

Chapter 7 – Dysferlinopathies

Robert H. Brown, A. Amato, Robert H. Brown, 2011 .

Disruption of muscle membrane and phenotype divergence in two novel mouse models of dysferlin deficiency.

Simon C Watkins, Robert H. Brown, L. Donahue, 2004, Human molecular genetics.

TDP-43 gains function due to perturbed autoregulation in a Tardbp knock-in mouse model of ALS-FTD

Matthew A. White, L. Saksida, T. Bussey, 2018, Nature Neuroscience.

Amyotrophic Lateral Sclerosis: An Emerging Era of Collaborative Gene Discovery

A. Singleton, J. Ostell, Robert H. Brown, 2007, PloS one.

Mice deficient in the Rab5 guanine nucleotide exchange factor ALS2/alsin exhibit age-dependent neurological deficits and altered endosome trafficking.

Robert H. Brown, S. Hadano, J. Shefner, 2006, Human molecular genetics.

No association of DYNC1H1 with sporadic ALS in a case‐control study of a northern European derived population: A tagging SNP approach

D. Goldstein, Robert H. Brown, K. Ahmadi, 2006, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

Juvenile Amyotrophic Lateral Sclerosis

Robert H. Brown, J. Sreedharan, Robert H. Brown, 2015 .

Mutant SPTLC1 dominantly inhibits serine palmitoyltransferase activity in vivo and confers an age-dependent neuropathy.

K. Gable, Robert H. Brown, J. Harmon, 2005, Human molecular genetics.

Sequence Variants in Human Neurofilament

Robert H. Brown, L. Bruijn, Zuoshang Xu, 1996 .

Suppression of mutant C9orf72 expression by a potent mixed backbone antisense oligonucleotide

Robert H. Brown, R. Bowser, D. Fabris, 2021, Nature Medicine.

Mutations in the N-terminal actin-binding domain of filamin C cause a distal myopathy.

Robert H. Brown, J. Landers, G. Ravenscroft, 2011, American journal of human genetics.

Identification of small subunits of mammalian serine palmitoyltransferase that confer distinct acyl-CoA substrate specificities

Gongshe Han, Sita D Gupta, K. Gable, 2009, Proceedings of the National Academy of Sciences.

Hereditary sensory neuropathy type 1 mutations confer dominant negative effects on serine palmitoyltransferase, critical for sphingolipid synthesis.

Robert H. Brown, S. Yasuda, K. Hanada, 2002, The Journal of clinical investigation.

Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis

Annelot M. Dekker, Raymond D. Schellevis, P. Visscher, 2016, Nature Genetics.

Cortical Spreading Depression Denotes Concussion Injury.

Robert H. Brown, C. Ayata, N. Henninger, 2019, Journal of neurotrauma.

A novel dysferlin mutant pseudoexon bypassed with antisense oligonucleotides

Robert H. Brown, M. Hegde, P. Sapp, 2014, Annals of clinical and translational neurology.

Age-Dependent TDP-43-Mediated Motor Neuron Degeneration Requires GSK3, hat-trick, and xmas-2

Robert H. Brown, M. Freeman, J. Sreedharan, 2015, Current Biology.

Ribonuclease 4 protects neuron degeneration by promoting angiogenesis, neurogenesis, and neuronal survival under stress

Robert H. Brown, J. Landers, G. Hu, 2013, Angiogenesis.

Intrinsic membrane hyperexcitability of amyotrophic lateral sclerosis patient-derived motor neurons.

Robert H. Brown, K. Eggan, G. Boulting, 2014, Cell reports.

Increase in the relative expression of tau with four microtubule binding repeat regions in frontotemporal lobar degeneration and progressive supranuclear palsy brains

Robert H. Brown, J. Growdon, B. Hyman, 2007, Acta Neuropathologica.

Identification of two novel loci for dominantly inherited familial amyotrophic lateral sclerosis.

J. Haines, M. Pericak-Vance, H. Horvitz, 2003, American journal of human genetics.

Rats Expressing Human Cytosolic Copper–Zinc Superoxide Dismutase Transgenes with Amyotrophic Lateral Sclerosis: Associated Mutations Develop Motor Neuron Disease

Robert H. Brown, Y. Itoyama, N. Kasai, 2001, The Journal of Neuroscience.

A gene encoding a putative GTPase regulator is mutated in familial amyotrophic lateral sclerosis 2

S. Scherer, Robert H. Brown, M. Hayden, 2001, Nature Genetics.

A novel locus for familial amyotrophic lateral sclerosis, on chromosome 18q.

Robert H. Brown, V. Meininger, F. Salachas, 2002, American journal of human genetics.

Lack of association between apolipoprotein E genotype and sporadic amyotrophic lateral sclerosis

J. Haines, M. Pericak-Vance, Robert H. Brown, 1998, Neurogenetics.

A genome-wide association meta-analysis identifies a novel locus at 17q11.2 associated with sporadic amyotrophic lateral sclerosis.

G. Comi, S. Corti, V. Moskvina, 2014, Human molecular genetics.

Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1.

Robert H. Brown, J. King, R. Bowser, 2016, Brain : a journal of neurology.

Mapping of Gene Expression Reveals CYP27A1 as a Susceptibility Gene for Sporadic ALS

Ewout J. N. Groen, S. Horvath, A. Hofman, 2012, PloS one.

Pathways disrupted in human ALS motor neurons identified through genetic correction of mutant SOD1.

Morgan L. Maeder, Derek H. Oakley, Mathew J. Goodwin, 2014, Cell stem cell.

Human genetics and neuropathology suggest a link between miR-218 and amyotrophic lateral sclerosis pathophysiology

O. Yizhar, Robert H. Brown, A. Al-Chalabi, 2019, Science Translational Medicine.

Mutant Profilin1 transgenic mice recapitulate cardinal features of motor neuron disease

Ashutosh Kumar Singh, Robert H. Brown, P. Ozdinler, 2016, Human molecular genetics.

Emerging mechanisms of molecular pathology in ALS.

Robert H. Brown, O. Peters, M. Ghasemi, 2015, The Journal of clinical investigation.

Prevalence of Huntington's disease gene CAG repeat alleles in sporadic amyotrophic lateral sclerosis patients

T. Gillis, J. Mysore, M. MacDonald, 2012, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

A randomized placebo‐controlled phase 3 study of mesenchymal stem cells induced to secrete high levels of neurotrophic factors in amyotrophic lateral sclerosis

N. Staff, Robert H. Brown, S. Lindborg, 2021, Muscle & nerve.

NurOwn, phase 2, randomized, clinical trial in patients with ALS

N. Staff, Robert H. Brown, M. Cudkowicz, 2019, Neurology.

XBP-1 deficiency in the nervous system protects against amyotrophic lateral sclerosis by increasing autophagy.

Robert H. Brown, C. Hetz, L. Glimcher, 2009, Genes & development.

amyotrophic lateral sclerosis by increasing autophagy XBP-1 deficiency in the nervous system protects against Material Supplemental

Robert H. Brown, C. Hetz, L. Glimcher, 2009 .

Mutations in the Profilin 1 Gene Cause Familial Amyotrophic Lateral Sclerosis

S. C. Chafe, D. Goldstein, Robert H. Brown, 2012, Nature.

Amyotrophic Lateral Sclerosis.

Robert H. Brown, A. Al-Chalabi, Robert H. Brown, 2017, The New England journal of medicine.

Discovery of a Biomarker and Lead Small Molecules to Target r(GGGGCC)-Associated Defects in c9FTD/ALS

Peter K. Todd, Robert H. Brown, L. Petrucelli, 2014, Neuron.

Association of UBQLN1 mutation with Brown–Vialetto–Van Laere syndrome but not typical ALS

Robert H. Brown, R. Tanzi, L. Bertram, 2012, Neurobiology of Disease.

Poly(Gp) Proteins Are A Useful Pharmacodynamic Marker For C9Orf72-Associated Amyotrophic Lateral Sclerosis

William T. Hu, Robert H. Brown, L. Petrucelli, 2017 .

Overexpression of the Wild-Type SPT1 Subunit Lowers Desoxysphingolipid Levels and Rescues the Phenotype of HSAN1

T. Hornemann, A. von Eckardstein, Anke Penno, 2009, The Journal of Neuroscience.

Amyotrophic lateral sclerosis: lessons from mouse and human genetics

Robert H. Brown, Robert H. Brown, 2001, Clinical Neuroscience Research.

Axonal Transport Defects in Neurodegenerative Diseases

Yuyu Song, Scott T. Brady, Klaus-Armin Nave, 2009, The Journal of Neuroscience.

Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways

Brittany N. Lasseigne, W. Chung, D. Goldstein, 2015, Science.

RNA metabolism and the pathogenesis of motor neuron diseases

Robert H. Brown, M. Moore, A. Al-Chalabi, 2010, Trends in Neurosciences.

Corticospinal Motor Neurons and Related Subcerebral Projection Neurons Undergo Early and Specific Neurodegeneration in hSOD1G93A Transgenic ALS Mice

Robert H. Brown, J. D. Macklis, P. H. Özdinler, 2011, The Journal of Neuroscience.

A large genome scan for rare CNVs in amyotrophic lateral sclerosis.

Ewout J. N. Groen, A. Hofman, A. Uitterlinden, 2010, Human molecular genetics.

ALS‐linked protein disulfide isomerase variants cause motor dysfunction

Robert H. Brown, P. Henny, M. Concha, 2016, The EMBO journal.

Identification of rare protein disulfide isomerase gene variants in amyotrophic lateral sclerosis patients.

Guy A Rouleau, Ute Woehlbier, Robert H. Brown, 2015, Gene.

Amyotrophic lateral sclerosis: Problems and prospects

Robert H. Brown, J. Sreedharan, Robert H. Brown, 2013, Annals of neurology.

Cytotoxicity of Botulinum Neurotoxins Reveals a Direct Role of Syntaxin 1 and SNAP-25 in Neuron Survival

Robert H. Brown, Hongyu Ruan, W. Yao, 2013, Nature Communications.

Age of onset of amyotrophic lateral sclerosis is modulated by a locus on 1p34.1

Carl D Langefeld, Aleksey Shatunov, Gabriele Mora, 2013, Neurobiology of Aging.

Variants of the elongator protein 3 (ELP3) gene are associated with motor neuron degeneration

R. Ophoff, H. Horvitz, P. Sham, 2008, Human molecular genetics.

Deleterious variants of FIG4, a phosphoinositide phosphatase, in patients with ALS.

Robert H. Brown, J. Landers, M. Meisler, 2009, American journal of human genetics.

No evidence for shared genetic basis of common variants in multiple sclerosis and amyotrophic lateral sclerosis.

R. Ophoff, A. Goris, S. Sawcer, 2014, Human molecular genetics.

Mutant Profilin 1 transgenic mice recapitulate cardinal features of motor neuron disease

Ashutosh Kumar Singh, Robert H. Brown, P. Ozdinler, 2017 .

ALS-associated missense and nonsense TBK1 mutations can both cause loss of kinase function

Robert H. Brown, F. Baas, A. Al-Chalabi, 2018, Neurobiology of Aging.

Endoplasmic reticulum stress leads to accumulation of wild-type SOD1 aggregates associated with sporadic amyotrophic lateral sclerosis

Robert H. Brown, D. A. Bosco, C. Hetz, 2018, Proceedings of the National Academy of Sciences.

Mutations in Cu/Zn superoxide dismutase (SOD1) are associated with familial amyotrophic lateral sclerosis (ALS)

Robert H. Brown, Robert H. Brown, 1993 .

Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability.

Robert H. Brown, B. van Zundert, P. Rojas, 2013, Journal of neurophysiology.

Mutational analysis reveals the FUS homolog TAF15 as a candidate gene for familial amyotrophic lateral sclerosis

Robert H. Brown, D. A. Bosco, C. Shaw, 2011, American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.

Silencing strategies for therapy of SOD1-mediated ALS

Robert H. Brown, B. Zundert, Robert H. Brown, 2017, Neuroscience Letters.

University of Groningen Mapping of Gene Expression Reveals CYP 27 A 1 as a Susceptibility Gene for Sporadic

Ewout J. N. Groen, S. Horvath, A. Hofman, 2012 .

Mutant PFN1 causes ALS phenotypes and progressive motor neuron degeneration in mice by a gain of toxicity

Eric W. Danielson, Robert H. Brown, J. Landers, 2016, Proceedings of the National Academy of Sciences.

Novel mutations support a role for Profilin 1 in the pathogenesis of ALS

Robert H. Brown, A. Al-Chalabi, C. Shaw, 2015, Neurobiology of Aging.

EPHA4 is a disease modifier of amyotrophic lateral sclerosis in animal models and in humans

A. Goris, Robert H. Brown, A. Al-Chalabi, 2012, Nature Medicine.

Mutational analysis of TARDBP in neurodegenerative diseases

Robert H. Brown, J. Landers, P. Keagle, 2011, Neurobiology of Aging.

A Yeast Model of FUS/TLS-Dependent Cytotoxicity

Daniel F Tardiff, G. Petsko, Robert H. Brown, 2011, PLoS biology.

CCNF mutations in amyotrophic lateral sclerosis and frontotemporal dementia

Robert H. Brown, R. Petersen, B. Boeve, 2016, Nature Communications.

A new approach for rare variation collapsing on functional protein domains implicates specific genic regions in ALS

Brittany N. Lasseigne, D. Goldstein, R. Myers, 2019, Genome research.

Regional Collapsing of Rare Variation Implicates Specific Genic Regions in ALS

Brittany N. Lasseigne, D. Goldstein, R. Myers, 2018, bioRxiv.

Title: Mutations in ANXA11 cause familial and sporadic amyotrophic lateral sclerosis

Robert H. Brown, M. Weale, F. Baas, 2016 .

Amyotrophic Lateral Sclerosis-Associated SOD1 Mutant Proteins Bind and Aggregate with Bcl-2 in Spinal Cord Mitochondria

Robert H. Brown, B. Hyman, B. Bacskai, 2004, Neuron.

BET bromodomain inhibitors PFI-1 and JQ1 are identified in an epigenetic compound screen to enhance C9ORF72 gene expression and shown to ameliorate C9ORF72-associated pathological and behavioral abnormalities in a C9ALS/FTD model

Robert H. Brown, M. Montecino, Nur Jury, 2021, Clinical epigenetics.

Reduced expression of the Kinesin-Associated Protein 3 (KIFAP3) gene increases survival in sporadic amyotrophic lateral sclerosis

R. Ophoff, H. Horvitz, S. Heath, 2009, Proceedings of the National Academy of Sciences.

A C9ORF72 BAC mouse model recapitulates key epigenetic perturbations of ALS/FTD

Robert H. Brown, C. Wahlestedt, M. Benatar, 2017, Molecular Neurodegeneration.

Widespread spinal cord transduction by intrathecal injection of rAAV delivers efficacious RNAi therapy for amyotrophic lateral sclerosis.

Robert H. Brown, Chunxing Yang, G. Gao, 2014, Human molecular genetics.

Small-molecule-mediated stabilization of familial amyotrophic lateral sclerosis-linked superoxide dismutase mutants against unfolding and aggregation.

Peter T Lansbury, Robert H. Brown, P. Lansbury, 2005, Proceedings of the National Academy of Sciences of the United States of America.

Multimodal Actions of Neural Stem Cells in a Mouse Model of ALS: A Meta-Analysis

R. Sidman, Robert H. Brown, J. Rothstein, 2012, Science Translational Medicine.

Apolipoprotein E is associated with age at onset of amyotrophic lateral sclerosis

J. Haines, M. Pericak-Vance, Robert H. Brown, 2004, Neurogenetics.

Apolipoprotein E ϵ4 allele is not associated with earlier age at onset in amyotrophic lateral sclerosis

Robert H. Brown, B. Hyman, D. McKenna-Yasek, 1995 .

Decreased Metallation and Activity in Subsets of Mutant Superoxide Dismutases Associated with Familial Amyotrophic Lateral Sclerosis* 210

Robert H. Brown, J. Valentine, A. Tiwari, 2002, The Journal of Biological Chemistry.

Low-level overexpression of wild type TDP-43 causes late-onset, progressive neurodegeneration and paralysis in mice

Robert H. Brown, H. Cai, Jia Yu, 2021, bioRxiv.

Randomized trial of l-serine in patients with hereditary sensory and autonomic neuropathy type 1

T. Hornemann, F. Eichler, Robert H. Brown, 2019, Neurology.

Pathogenic Huntingtin Repeat Expansions in Patients with Frontotemporal Dementia and Amyotrophic Lateral Sclerosis.

Timothy A. Miller, Sonja W. Scholz, Jennifer E. Phillips-Cremins, 2020, Neuron.

Non-Coding Genetic Analysis Implicates Interleukin 18 Receptor Accessory Protein 3′UTR in Amyotrophic Lateral Sclerosis

Ashley R. Jones, E. Segal, Robert H. Brown, 2021, bioRxiv.

Mutations in neurofilament genes are not a significant primary cause of non-SOD1-mediated amyotrophic lateral sclerosis

D. Hernandez, A. Singleton, Robert H. Brown, 2006, Neurobiology of Disease.

ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2

Robert H. Brown, P. Pasinelli, D. Trotti, 2010, Human molecular genetics.

ERBB4 mutations that disrupt the neuregulin-ErbB4 pathway cause amyotrophic lateral sclerosis type 19.

Robert H. Brown, A. Fujiyama, A. Toyoda, 2013, American journal of human genetics.

Metabolic Dysfunction in Familial, but Not Sporadic, Amyotrophic Lateral Sclerosis

M. Gurney, Robert H. Brown, M. Beal, 1998, Journal of neurochemistry.

Variant-selective stereopure oligonucleotides protect against pathologies associated with C9orf72-repeat expansion in preclinical models

Robert H. Brown, K. Longo, J. Dodart, 2021, Nature Communications.

Association of a Locus in the CAMTA1 Gene With Survival in Patients With Sporadic Amyotrophic Lateral Sclerosis.

Sandra D'Alfonso, Adriano Chiò, Aleksey Shatunov, 2016, JAMA neurology.

Association of a Locus in the CAMTA 1 GeneWith Survival in PatientsWith Sporadic Amyotrophic Lateral Sclerosis

Adriano Chiò, Philip Van Damme, Aleksey Shatunov, 2016 .

Signaling myopia

K. Narasimhan, M. Hediger, I. Russell, 1999, Nature Neuroscience.

Anti-superoxide dismutase antibodies are associated with survival in patients with sporadic amyotrophic lateral sclerosis

Robert H. Brown, B. Hyman, D. A. Bosco, 2011, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

Superoxide dismutase in familial amyotrophic lateral sclerosis: models for gain of function

Robert H. Brown, Robert H. Brown, 1995, Current Opinion in Neurobiology.

An open label study of a novel immunosuppression intervention for the treatment of amyotrophic lateral sclerosis

Robert H. Brown, D. Schoenfeld, J. Glass, 2018, Amyotrophic lateral sclerosis & frontotemporal degeneration.

Longitudinal biomarkers in amyotrophic lateral sclerosis

Robert H. Brown, K. Scearce-Levie, J. Glass, 2020, Annals of clinical and translational neurology.

Analysis of factors that modify susceptibility and rate of progression in amyotrophic lateral sclerosis (ALS)

Robert H. Brown, M. Cudkowicz, D. Hayden, 2006, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

Screening for inhibitors of the SOD1 gene promoter: Pyrimethamine does not reduce SOD1 levels in cell and animal models

Robert H. Brown, M. Glicksman, M. Huang, 2010, Neuroscience Letters.

Quantifying and Mitigating Motor Phenotypes Induced by Antisense Oligonucleotides in the Central Nervous System

Robert H. Brown, J. Watts, K. Fitzgerald, 2021, bioRxiv.

Absence of mutations in the Mn superoxide dismutase or catalase genes in familial amyotrophic lateral sclerosis

Robert H. Brown, G. Rouleau, J. Parboosingh, 1995, Neuromuscular Disorders.

Mutant Sod1-expressing Astrocytes Release Toxic Factors That Trigger Motor Neuron Death

F. R. Mir, D. Gonzalez, Van Zundert, 2013 .

Identification of two novel mutations and a new polymorphism in the gene for Cu/Zn superoxide dismutase in patients with amyotrophic lateral sclerosis.

H. Horvitz, M. Beal, P. Sapp, 1994, Human molecular genetics.

Novel mutation in VCP gene causes atypical amyotrophic lateral sclerosis

D. Goldstein, Robert H. Brown, A. Fox, 2012, Neurology.

Motor unit number estimation predicts disease onset and survival in a transgenic mouse model of amyotrophic lateral sclerosis

Merit Cudkowicz, Robert H. Brown, M. Cudkowicz, 2006, Muscle & nerve.

Ribonuclease 4 protects neuron degeneration by promoting angiogenesis, neurogenesis, and neuronal survival under stress

J. Landers, G. Hu, J. Sheng, 2012, Angiogenesis.

Genetic ablation of phospholipase C delta 1 increases survival in SOD1G93A mice

A. Al-Chalabi, W. Robberecht, A. Shatunov, 2013, Neurobiology of Disease.

A high-throughput screen to identify inhibitors of SOD1 transcription.

Robert H. Brown, R. Ferrante, W. Matson, 2012, Frontiers in bioscience.

A large genome scan for rare CNVs in amyotrophic lateral sclerosis.

Ewout J. N. Groen, L. Wain, M. Tobin, 2010, Human molecular genetics.

Mutant SOD1 protein increases Nav1.3 channel excitability

William R. Kobertz, Robert H. Brown, W. R. Kobertz, 2016, Journal of Biological Physics.

Mutant FUS proteins that cause amyotrophic lateral sclerosis incorporate into stress granules.

D. A. Bosco, L. Hayward, P. Sapp, 2010, Human molecular genetics.

C9orf72 and UNC13A are shared risk loci for amyotrophic lateral sclerosis and frontotemporal dementia: A genome‐wide meta‐analysis

P. D. Bakker, F. Rivadeneira, A. Al-Chalabi, 2014, Annals of neurology.

Potent Mixed Backbone Antisense Oligonucleotide Safety Suppressed Expression of Mutant C9ORF72 Transcripts and Polypeptides: First in Human Pilot Study

Robert H. Brown, R. Bowser, D. Fabris, 2021 .

A novel dysferlin mutant pseudoexon bypassed with antisense oligonucleotides

M. Hegde, P. Sapp, J. Dominov, 2014, Annals of clinical and translational neurology.

NEK1 variants confer susceptibility to amyotrophic lateral sclerosis

Annelot M. Dekker, F. Baas, T. Meitinger, 2016, Nature Genetics.

Medications and laboratory parameters as prognostic factors in amyotrophic lateral sclerosis

Robert H. Brown, D. Schoenfeld, A. Dibernardo, 2008, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

Evaluation of the Golgi trafficking protein VPS54 (wobbler) as a candidate for ALS

S. Ennis, Robert H. Brown, O. Hardiman, 2008, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

Silencing strategies for therapy of SOD1-mediated ALS

B. Zundert, Robert H. Brown, 2017, Neuroscience Letters.

A randomized trial of mexiletine in ALS

Robert H. Brown, A. Pestronk, D. Greenblatt, 2016, Neurology.

ASO5-1 C9ORF72 Manuscript – 05Feb2021 POTENT MIXED BACKBONE ANTISENSE OLIGONUCLEOTIDE SAFELY SUPPRESSES EXPRESSION OF MUTANT C9ORF72 TRANSCRIPTS AND POLYDIPEPTIDES: FIRST IN HUMAN PILOT STUDY

Robert H. Brown, R. Bowser, D. Fabris, 2021 .

Nucleic Acid Therapeutics for Neurological Diseases

A. Khvorova, J. Watts, Robert H. Brown, 2019, Neurotherapeutics.

Intralingual and Intrapleural AAV Gene Therapy Prolongs Survival in a SOD1 ALS Mouse Model

Robert H. Brown, C. Mueller, M. ElMallah, 2019, Molecular therapy. Methods & clinical development.

Therapeutic rAAVrh10 Mediated SOD1 Silencing in Adult SOD1G93A Mice and Nonhuman Primates

Robert H. Brown, C. Mueller, M. ElMallah, 2015, Human gene therapy.

Therapeutic rAAVrh 10 Mediated SOD 1 Silencing in Adult SOD 1 ( G 93 A ) Mice and Nonhuman Primates

Robert H. Brown, C. Mueller, M. ElMallah, 2017 .

Thrombopoietin is ineffective in a mouse model of motor neuron disease

Robert H. Brown, M. Cudkowicz, A. Caraganis, 2008, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

No evidence for shared genetic basis of common variants in multiple sclerosis and amyotrophic lateral sclerosis.

R. Ophoff, A. Goris, S. Sawcer, 2014, Human molecular genetics.

Paraoxonase gene mutations in amyotrophic lateral sclerosis

Robert H. Brown, D. A. Bosco, J. Glass, 2010, Annals of neurology.

Defective daily temperature regulation in a mouse model of amyotrophic lateral sclerosis

Robert H. Brown, S. Swoap, W. Schwartz, 2019, Experimental Neurology.

Mutations in the Profilin 1 Gene Cause Familial Amyotrophic Lateral Sclerosis

S. C. Chafe, D. Goldstein, M. Moore, 2012, Nature.

Two Approaches to Drug Discovery in SOD1-Mediated ALS

Robert H. Brown, M. Glicksman, A. Kazantsev, 2006, Journal of biomolecular screening.

Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis

Annelot M. Dekker, Raymond D. Schellevis, Ashley R. Jones, 2016, Nature Genetics.

Cortical Spreading Depression Denotes Concussion Injury.

C. Ayata, N. Henninger, J. Bouley, 2019, Journal of neurotrauma.

Endogenous retroviruses in ALS: A reawakening?

Robert H. Brown, A. Al-Chalabi, Robert H. Brown, 2015, Science Translational Medicine.

RNA interference-mediated silencing of mutant superoxide dismutase rescues cyclosporin A-induced death in cultured neuroblastoma cells.

Robert H. Brown, A. Kazantsev, P. Pasinelli, 2004, Proceedings of the National Academy of Sciences of the United States of America.