KOL Resume for Benjamin Rix Brooks (spinal, neuron, disease, motor, atrophy, motor neuron disease, muscular)
Atrium Health Neurosciences Institute, Carolinas Medical Center, University of North Carolina School of Medicine–Charlotte Campus, Charlotte, North Carolina, United States of America
Clinical Trials Planning LLC, NC, USA
Atrium Health Neurosciences Institute, Carolinas Medical Center, University of North Carolina School of Medicine, Charlotte, NC, USA, and.
Atrium Health Neurosciences Institute, University of North Carolina School of Medicine, Charlotte, NC, USA, View further author information
Carolinas Medical Center, Charlotte, NC, U.S.A.
Neurosciences Institute, Atrium Health, University of North Carolina School of Medicine, Charlotte, NC 28203, USA
Department of Neurology, Neuroscience and Spine Institute, Carolinas Medical Center, Carolinas Neuromuscular/ALS-MDA Center, Charlotte, NC, USA;, View further author information
Neuroscience Institute – Neurology, Carolinas Neuromuscular/ALS-MDA Center, Carolinas Healthcare System, Charlotte, NC
a Neurology Department , Carolinas Medical Center , Charlotte , North Carolina , USA.
University of North Carolina School of Medicine–Charlotte Campus, Charlotte, NC
Carolinas Medical Center, Charlotte, NC
University of North Carolina School of Medicine, Charlotte Campus, Charlotte, NC, 28203, USA
Carolinas Neuromuscular/ALS-MDA Center, Department of Neurology, Carolinas Medical Center, Charlotte, NC 28203, USA
From the Division of Neuromuscular Medicine (J.Y., H.-X.D., N.S., F.F., W.C., Y.Y., E.L., S.D., J.G.Z., Y.S., K.B.A., T.S.), Davee Department of Neurology and Clinical Neurosciences, Northwestern University Feinberg School of Medicine, Chicago, IL; Department of Neurology (B.B.), Neuroscience and Spine Institute, Carolinas Medical Center, Charlotte, NC; and USC Neuromuscular Center (W.K.E.), Good Samaritan Hospital, Los Angeles, CA.
Carolinas Neuromuscular/ALS-MDA Center, Department of Neurology, Neuroscience and Spine Institute, Carolinas Medical Center, Charlotte, NC
Cannon Research Center, Carolinas Medical Center, Charlotte, North Carolina 28203
Department of Neurology, Carolinas Neuromuscular/ALS-MDA Center, Neuroscience and Spine Institute, Carolinas Medical Center, 1010 Edgehill Road North, Charlotte, NC 28207-1885, USA
University of Wisconsin School of Medicine and Public Health, Madison, WI; and Carolinas Neuromuscular/Amyotrophic Lateral Sclerosis‐Muscular Dystrophy Association Center, Charlotte, NC
Dr. Brooks is professor of neurology and director MDA/ALS Clinical Research Center at the, University of Wisconsin
Benjamin R. Brooks, MD, is professor of neurology in the Department of Neurology at the, University of Wisconsin, Madison
Department of Neurology, University of Miami School of Medicine (M712), PO Box 016990, Miami, Florida 33101, USA
Department of Neurology, University of Wisconsin-Madison, Madison, USA
ALS Clinic, Madison, WI, USA
Neurology and Research Services, William S. Middleton Memorial Veterans Affairs Medical Center, and Neurology and Medical Microbiology Departments, University of Wisconsin—Madison Medical School, Madison, Wisconsin 53705-2286
University of Wisconsin Hospital & Clinics ALS Clinical Research Center and William S Middleton Memorial Veterans Affairs Medical Center Great Lakes Veterans Integrated Service Network (VISN 12), Madison, Wisconsin, USA
Conference Organizer for WFN Research Committee on Motor Neuron Diseases
American Academy of Neurology, 1080 Montreal Ave., St. Paul, MN 55116
ALS Clinical Research Center, University of Wisconsin Hospital and Clinics, Clinical Science Center H6-563, 600 Highland Avenue, Madison, WI 53972-5132, USA
Dept. of Neurology, USA
Chicago, IL (Teepu Siddique, Hong); Madison, WI (Brooks); Chicago, IL(Hung, N.A. Siddique); Durham, NC (Rimmler); Chicago, IL (Kaplan); Nashville, TN (Haines); Boston, MA (Brown); Durham, NC. (Pericak)
From the University of Wisconsin ALS Clinical Research Center, Neurology Service, William S. Middleton Memorial VA Medical Center, Great Lakes Veterans Integrated Service Network, Madison, WI. Address correspondence and reprint requests to Dr. B.R. Brooks, Director, ALS Clinic and ALS Clinical Research Center, University of Wisconsin Hospital and Clinics, Department of Neurology, 600 Highland Ave., Madison, WI 53792.
Neuromuscular Unit, Neurology Department, Madison, WI.
Neurology Service, William S. Middleton Memorial VA Medical Center, Madison, Wisconsin, USA
From the ALS Clinical Research Center, University of Wisconsin Hospital and Clinics and William S. Middleton Memorial Veterans Hospital, Great Lakes Veterans Integrated Service Network (12), Madison, WI. Address correspondence and reprint requests to Dr. Benjamin Rix Brooks, ALS Clinical Research Center, University of Wisconsin Hospital and Clinics, 600 Highland Avenue CSC H6-558, Madison, WI 53792-5132. This work was supported in part by the Muscular Dystrophy Association, US Public Health Service General Clinical Research Center grant M01RR03186, a program grant for Medical Student Biomedical Research and the Department of Veterans Affairs General Research, Education and Clinical Center grant.
Neurology Service, William S. Middleton Memorial VA Medical Center, Madison, Wisconsin, USA.
Neurology Service, William S. Middleton Memorial Veterans Affairs Hospital.
ALS Clinical Research Center, University of Wisconsin Hospital and Clinics, Madison 53792-5132, USA.
ALS Clinical Research Center University of Wisconsin Hospital and Clinics Clinical Science Center J6-504 Madison, WI 53792-5132, USA Tel.: (608) 263-9057 Fax: (608) 263-0412
Neurology Department, Medical School University of Wisconsin, Madison, WI 53705-2280, U.S.A.
Department of Neurology/127, Wm. S. Middleton Memorial, Veterans Hospital, Madison, WI 53705
University of Texas M. D. Anderson Cancer Center, Smithville 78957.
Department of Neurology Center for Health Sciences University of Wisconsin-Madison, and Neurology Service Veterans Administration Hospital Madison, WI
Department of Neurology Center for Health Sciences University of Wisconsin-Madison
University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville 78957
Department of Neurology, Center for Health Sciences University of Wisconsin-Madison
Departments of Neurology and Medical Microbiology, University of Wisconsin Medical School, Madison, WI 53792 U.S.A.
Treatment Center University of Wisconsin Hospital and Clinics Clinical Science Center J6–504 Madison, Wisconsin 53792
Department of Neurology, Center for Health Sciences, University of Wisconsin-Madison
Prominent publications by Benjamin Rix Brooks
Safety and efficacy of ceftriaxone for amyotrophic lateral sclerosis: a multi-stage, randomised, double-blind, placebo-controlled trial
[ PUBLICATION ]
BACKGROUND: Glutamate excitotoxicity might contribute to the pathophysiology of amyotrophic lateral sclerosis. In animal models, decreased excitatory aminoacid transporter 2 (EAAT2) overexpression delays disease onset and prolongs survival, and ceftriaxone increases EAAT2 activity. We aimed to assess the safety and efficacy of ceftriaxone for amyotrophic lateral sclerosis in a combined phase 1, 2, and 3 clinical trial.
METHODS: This three-stage randomised, double-blind, ...
|Known for Amyotrophic Lateral Sclerosis | Placebo Participants | Animal Models | Glutamate Excitotoxicity | Clinical Trial|
Mutations in UBQLN2 cause dominant X-linked juvenile and adult onset ALS and ALS/dementia
[ PUBLICATION ]
Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neuron degeneration in the brain and spinal cord. Most cases of ALS are sporadic but about 5-10% are familial. Mutations in superoxide dismutase 1 (SOD1), TAR DNA-binding protein (TARDBP, also known as TDP43) and fused in sarcoma (FUS, also known as translocated in liposarcoma (TLS)) account for approximately 30% of classic familial ALS. Mutations in several other genes have also been reported ...
|Known for Mutations Ubqln2 | Adult Onset | Dominant Genes | Proteins Dementia | Superoxide Dismutase|
Frameshift and novel mutations in FUS in familial amyotrophic lateral sclerosis and ALS/dementia(e–Pub ahead of print)
[ PUBLICATION ]
OBJECTIVE: Amyotrophic lateral sclerosis (ALS) is a progressive paralytic disorder caused by degeneration of motor neurons. Mutations in the FUS gene were identified in patients with familial ALS (FALS) and patients with sporadic ALS (SALS) from a variety of genetic backgrounds. This work further explores the spectrum of FUS mutations in patients with FALS and patients with FALS with features of frontotemporal dementia (FALS/FTD) or parkinsonism and dementia (FALS/PD/DE).
METHODS: All ...
|Known for Fus Mutations | Patients Fals | Amyotrophic Lateral | Bulbar Onset | Motor Neurons|
Alteration from T- to B-cell tropism reduces thymic atrophy and cytocidal effects in thymocytes but not neurovirulence induced by ts1, a mutant of Moloney murine leukemia virus TB.
[ PUBLICATION ]
The ts1 mutant of Moloney murine leukemia virus TB causes degenerative neurologic and immunologic disease in mice, characterized by development of spongiform encephalomyelopathy resulting in hindlimb paralysis, marked thymic atrophy associated with immunodeficiency, and generalized body wasting. To investigate the pathogenesis of the thymic atrophy caused by ts1, we constructed a chimeric virus, ts1-Cas(NS), in which a major portion of the U3 region of the long terminal repeat of ts1, a ...
|Known for Leukemia Virus | Thymic Atrophy | Moloney Murine | Mice Ts1 | U3 Region|
Correlation of specific virus-astrocyte interactions and cytopathic effects induced by ts1, a neurovirulent mutant of Moloney murine leukemia virus.
[ PUBLICATION ]
ts1 is a highly neuropathogenic and lymphocytopathic mutant of Moloney murine leukemia virus TB (MoMuLV-TB). We previously reported that the primary neuropathogenic determinant of ts1 maps to a single amino acid substitution, Val-25-->Ile, in precursor envelope protein gPr80env. This Val-25-->Ile substitution apparently renders gPr80env inefficient for transport from the endoplasmic reticulum to the Golgi apparatus. These findings suggest that the cytopathic effect of ts1 in neural cells ...
|Known for Leukemia Virus | Moloney Murine | Cytopathic Effects | Ts1 Momulv | Endoplasmic Reticulum|
BACKGROUND: Patients with ALS commonly exhibit pseudobulbar affect.
METHODS: The authors conducted a multicenter, randomized, double-blind, controlled, parallel, three-arm study to test a defined combination of dextromethorphan hydrobromide (DM) and quinidine sulfate (Q) (AVP-923) for the treatment of pseudobulbar affect in ALS. Q inhibits the rapid first-pass metabolism of DM. The effects of AVP-923 (30 mg of DM plus 30 mg of Q) given twice daily for 28 days were compared with those of ...
|Known for Pseudobulbar Affect | 30 Dm | Quality Life | Cytochrome P450 | Inhibitors Dextromethorphan|
PRISM: A Novel Research Tool to Assess the Prevalence of Pseudobulbar Affect Symptoms across Neurological Conditions
[ PUBLICATION ]
BACKGROUND: Pseudobulbar affect (PBA) is a neurological condition characterized by involuntary, sudden, and frequent episodes of laughing and/or crying, which can be socially disabling. Although PBA occurs secondary to many neurological conditions, with an estimated United States (US) prevalence of up to 2 million persons, it is thought to be under-recognized and undertreated. The PBA Registry Series (PRISM) was established to provide additional PBA symptom prevalence data in a large, ...
|Known for Neurological Conditions | Pba Symptoms | Pseudobulbar Affect | Multiple Sclerosis | Cns Score|
The Neuromediator Glutamate, through Specific Substrate Interactions, Enhances Mitochondrial ATP Production and Reactive Oxygen Species Generation in Nonsynaptic Brain Mitochondria*
[ PUBLICATION ]
The finding that upon neuronal activation glutamate is transported postsynaptically from synaptic clefts and increased lactate availability for neurons suggest that brain mitochondria (BM) utilize a mixture of substrates, namely pyruvate, glutamate, and the tricarboxylic acid cycle metabolites. We studied how glutamate affected oxidative phosphorylation and reactive oxygen species (ROS) production in rat BM oxidizing pyruvate + malate or succinate. Simultaneous oxidation of glutamate + ...
|Known for Brain Mitochondria | Reactive Oxygen | Ros Generation | Atp Production | Serum Albumin|
Deciphering amyotrophic lateral sclerosis: What phenotype, neuropathology and genetics are telling us about pathogenesis
[ PUBLICATION ]
Amyotrophic lateral sclerosis (ALS) is characterized phenotypically by progressive weakness and neuropathologically by loss of motor neurons. Phenotypically, there is marked heterogeneity. Typical ALS has mixed upper motor neuron (UMN) and lower motor neuron (LMN) involvement. Primary lateral sclerosis has predominant UMN involvement. Progressive muscular atrophy has predominant LMN involvement. Bulbar and limb ALS have predominant regional involvement. Frontotemporal dementia has ...
|Known for Lateral Sclerosis | Motor Neurons | Lmn Involvement | Multiple Phenotypes | Frontotemporal Dementia|
Efficacy and safety of xaliproden in amyotrophic lateral sclerosis: results of two phase III trials
[ PUBLICATION ]
Amyotrophic lateral sclerosis (ALS) is a relentlessly progressive and fatal motor neuron disease. We carried out two randomized, double-blind, placebo-controlled, multi-centre, multi-national studies with xaliproden (a drug with neurotrophic effect) to assess drug efficacy and safety at two doses. Patients with clinically probable or definite ALS of more than 6 months and less than 5 years duration were randomly assigned to placebo, 1 mg or 2 mg xaliproden orally once daily as ...
|Known for Amyotrophic Lateral | Phase Iii Trials | Primary Endpoints | 1 2 | Permanent Assisted Ventilation|
Hypercaloric enteral nutrition in patients with amyotrophic lateral sclerosis: a randomised, double-blind, placebo-controlled phase 2 trial
[ PUBLICATION ]
BACKGROUND: Amyotrophic lateral sclerosis is a fatal neurodegenerative disease with few therapeutic options. Mild obesity is associated with greater survival in patients with the disease, and calorie-dense diets increased survival in a mouse model. We aimed to assess the safety and tolerability of two hypercaloric diets in patients with amyotrophic lateral sclerosis receiving enteral nutrition.
METHODS: In this double-blind, placebo-controlled, randomised phase 2 clinical trial, we ...
|Known for Amyotrophic Lateral Sclerosis | Enteral Nutrition | Tolerability Patients | Diet Hf | Randomised Controlled|
Motor fatigue is a common complaint in patients with amyotrophic lateral sclerosis (ALS), but is often excluded, unlike weakness, from the clinical assessment of these patients. This could be due to the complexity and often painful assessment techniques of this motor deficit. This study examines the feasibility of quantitative assessment of motor fatigue by modifying presently available force measurements. The relationship between weakness and fatigue in ALS patients was also examined. ...
|Known for Motor Fatigue | Amyotrophic Lateral Sclerosis | Quantitative Assessment | Normal Control | Common Complaint|
In Vitro Effects of Cholesterol β-d-Glucoside, Cholesterol and Cycad Phytosterol Glucosides on Respiration and Reactive Oxygen Species Generation in Brain Mitochondria
[ PUBLICATION ]
The cluster of neurodegenerative disorders in the western Pacific termed amyotrophic lateral sclerosis–parkinsonism dementia complex (ALS-PDC) has been repeatedly linked to the use of seeds of various species of cycad. Identification and chemical synthesis of the most toxic compounds in the washed cycad seeds, a variant phytosteryl glucosides, and even more toxic cholesterol β-d-glucoside (CG), which is produced by the human parasite Helicobacter pylori, provide a possibility to study in ...
|Known for Vitro Effects | Oxygen Species | Ros Production | Mitochondrial Functions | Stigmasterol Β|
Benjamin Rix Brooks: Influence Statistics
|bloodbrain barrier subject||#1|
|1 95 scores||#1|
|alsfrsr scores baseline||#1|
|level hm dna||#1|
|combatals study design||#1|
|neurons consistent finding||#1|
|incomplete physical forms||#1|
|hormone metabolism alter||#1|
|microarray analysis leukocytes||#1|
|vestibular deficits disequilibrium||#1|
|edaravone study 19||#1|
|abnormal mbp levels||#1|
|neuropathogenic variant moloney||#1|
|hm dna molecules||#1|
|outcome measures stage||#1|
|reldesemtiv 12 weeks||#1|
|manifestation myoelectrical fatigue||#1|
|ambulatory function stages||#1|
|clinical trials determination||#1|
|repetitive rhythmic exercise||#1|
|cyclic nucleotide alterations||#1|
|elevated mbp levels||#1|
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Key People For Amyotrophic Lateral Sclerosis
Benjamin Rix Brooks:Expert Impact
Concepts for whichBenjamin Rix Brookshas direct influence:Amyotrophic lateral sclerosis, Amyotrophic lateral, Lateral sclerosis, Spinal cord, Cerebrospinal fluid, Leukemia virus, Cerebellar stimulation, Multiple sclerosis.
Benjamin Rix Brooks:KOL impact
Concepts related to the work of other authors for whichfor which Benjamin Rix Brooks has influence:Amyotrophic lateral sclerosis, Frontotemporal dementia, Motor neuron, Spinal cord, Neurodegenerative diseases, Cognitive impairment, Central nervous.
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