Spinal Muscular Atrophy (SMA) Biomarkers Study in the Immediate Postnatal Period of Development

NCT ID: NCT01736553

Last Updated: 2018-05-04

Study Results

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Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

53 participants

Study Classification

OBSERVATIONAL

Study Start Date

2012-12-31

Study Completion Date

2015-09-30

Brief Summary

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Spinal muscular atrophy (SMA) is the leading genetic cause of death of infants. Strong preclinical evidence suggests that effective therapy must be delivered as early as possible to prevent progression of the disease. The primary study objective will be to identify prognostic and surrogate biomarkers of disease progression that will facilitate the execution of therapeutic SMA clinical trials in infants.

Detailed Description

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Aim 1. To establish the validity of putative physiological SMA biomarkers in the immediate postnatal period. A longitudinal, natural history examination of physiological markers of muscle innervation will be performed in healthy and SMA infants. The first week of life is the ideal first time point, with visits occurring at scheduled visits up to the age two. Compound motor action potential (CMAP) amplitude and electrical impedance myography (EIM) will be examined and will be correlated with motor function. Each of these is associated with muscle innervation and provides information on the number and function of lower motor neurons in the spinal cord, the cellular target of SMA therapeutic interventions. This trial will establish the natural history of these putative SMA biomarkers as the disease evolves in affected infants. Moreover, our approach will allow for measurements in pre-symptomatic and early symptomatic subjects and determine their predictive value.

Aim 2. To establish the validity of putative molecular SMA biomarkers in the immediate postnatal period. Survival Motor Neuron (SMN2) copy number is a valid, predictive molecular SMA biomarker; however, it is fixed, and therefore not useful as a biomarker of clinical progression or response to therapy. SMN messenger Ribonucleic acid (mRNA) ( and protein expression is variable in different cell types and, in mice, naturally decreases with age postnatally. In this study, SMN expression levels will be measured longitudinally in SMA patients and controls. Additional putative molecular SMA markers that have been identified to correlate with motor function will be determined in an effort to distinguish between predictive markers that change prior to development of weakness and those that change as a consequence of weakness.

Conditions

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Spinal Muscular Atrophy (SMA)

Study Design

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Observational Model Type

COHORT

Study Time Perspective

PROSPECTIVE

Study Groups

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Infants with Spinal Muscular Atrophy

Infants diagnosed Spinal Muscular Atrophy

No interventions assigned to this group

Healthy controls

Healthy control infants

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

All infants will be between 0-6 months of age at the time of enrollment. Parents or guardians of the enrolled infants must sign an informed consent form prior to any study procedure being performed.

The infants with SMA must have already had a positive DNA test outside of the study to qualify for enrollment. An infant with SMA can have any number of SMN2 gene copies. Knowledge of the number of SMN2 gene copies prior to enrollment is not required.

Healthy control infants who meet the following criteria will be enrolled:

* Birth between 36 and 42 weeks inclusive of gestation
* Siblings of children with SMA must have had prior SMA genetic testing completed con-firming the infant is a healthy control
* Principal investigator feels the family/infant is able and willing to comply with study procedures
* Parent or guardian able to give informed consent

SMA infants who meet the following criteria will be enrolled:

* Birth between 36 and 42 weeks inclusive of gestation
* Positive SMN1 gene mutation/deletion
* Principal investigator feels the family/infant is able and willing to comply with study procedures
* Parent or guardian able to give informed consent

Exclusion Criteria

* Use of any putative therapy intended to increase the amount of SMN protein in cells
* Enrollment in an SMA therapeutic trial at the time of enrollment in the SMA biomarker study
* Have a systemic illness requiring ongoing treatment, such as pneumonia
* Clinically significant abnormal findings (as determined by the investigator) on the physical examination or medical history (including history of tracheostomy tubes and ventilator-dependency)
* Dependency upon non-invasive ventilatory support (ie: BiPAP) for more than 12 hours/day
Maximum Eligible Age

6 Months

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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National Institute of Neurological Disorders and Stroke (NINDS)

NIH

Sponsor Role collaborator

Cure SMA

OTHER

Sponsor Role collaborator

Massachusetts General Hospital

OTHER

Sponsor Role collaborator

University of Iowa

OTHER

Sponsor Role collaborator

Ohio State University

OTHER

Sponsor Role lead

Responsible Party

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Stephen J. Kolb

Prinicipal Investigator of NeuroNEXT

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Stephen J Kolb, MD PhD

Role: PRINCIPAL_INVESTIGATOR

Ohio State University

Locations

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University of California - Davis

Davis, California, United States

Site Status

University of California - Los Angeles

Los Angeles, California, United States

Site Status

Children's Hospital Colorado

Aurora, Colorado, United States

Site Status

Children's National Medical Center

Washington D.C., District of Columbia, United States

Site Status

Ann & Robert H. Lurie Children's Hospital of Chicago

Chicago, Illinois, United States

Site Status

Boston Children's Hospital

Boston, Massachusetts, United States

Site Status

Children's Mercy Hospital

Kansas City, Missouri, United States

Site Status

Washington University in St. Louis School of Medicine

St Louis, Missouri, United States

Site Status

Columbia University Medical Center

New York, New York, United States

Site Status

State University of New York Upstate Medical Center

Syracuse, New York, United States

Site Status

Nationwide Children's Hospital

Columbus, Ohio, United States

Site Status

Doernbecher Children's Hospital

Portland, Oregon, United States

Site Status

Vanderbilt University

Nashville, Tennessee, United States

Site Status

Children's Medical Center of Dallas

Dallas, Texas, United States

Site Status

University of Utah Health Sciences Center

Salt Lake City, Utah, United States

Site Status

Countries

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United States

References

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Campbell SK, Swanlund A, Smith E, Liao PJ, Zawacki L. Validity of the TIMPSI for estimating concurrent performance on the test of infant motor performance. Pediatr Phys Ther. 2008 Spring;20(1):3-10. doi: 10.1097/PEP.0b013e31815f66a6.

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Hua Y, Sahashi K, Hung G, Rigo F, Passini MA, Bennett CF, Krainer AR. Antisense correction of SMN2 splicing in the CNS rescues necrosis in a type III SMA mouse model. Genes Dev. 2010 Aug 1;24(15):1634-44. doi: 10.1101/gad.1941310. Epub 2010 Jul 12.

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Kolb SJ, Gubitz AK, Olszewski RF Jr, Ottinger E, Sumner CJ, Fischbeck KH, Dreyfuss G. A novel cell immunoassay to measure survival of motor neurons protein in blood cells. BMC Neurol. 2006 Feb 1;6:6. doi: 10.1186/1471-2377-6-6.

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Kolb SJ, Kissel JT. Spinal muscular atrophy: a timely review. Arch Neurol. 2011 Aug;68(8):979-84. doi: 10.1001/archneurol.2011.74. Epub 2011 Apr 11.

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Lutz CM, Kariya S, Patruni S, Osborne MA, Liu D, Henderson CE, Li DK, Pellizzoni L, Rojas J, Valenzuela DM, Murphy AJ, Winberg ML, Monani UR. Postsymptomatic restoration of SMN rescues the disease phenotype in a mouse model of severe spinal muscular atrophy. J Clin Invest. 2011 Aug;121(8):3029-41. doi: 10.1172/JCI57291. Epub 2011 Jul 25.

Reference Type BACKGROUND
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Morton JP, MacLaren DP, Cable NT, Bongers T, Griffiths RD, Campbell IT, Evans L, Kayani A, McArdle A, Drust B. Time course and differential responses of the major heat shock protein families in human skeletal muscle following acute nondamaging treadmill exercise. J Appl Physiol (1985). 2006 Jul;101(1):176-82. doi: 10.1152/japplphysiol.00046.2006. Epub 2006 Mar 24.

Reference Type BACKGROUND
PMID: 16565353 (View on PubMed)

Narver HL, Kong L, Burnett BG, Choe DW, Bosch-Marce M, Taye AA, Eckhaus MA, Sumner CJ. Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition. Ann Neurol. 2008 Oct;64(4):465-70. doi: 10.1002/ana.21449.

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Passini MA, Bu J, Richards AM, Kinnecom C, Sardi SP, Stanek LM, Hua Y, Rigo F, Matson J, Hung G, Kaye EM, Shihabuddin LS, Krainer AR, Bennett CF, Cheng SH. Antisense oligonucleotides delivered to the mouse CNS ameliorate symptoms of severe spinal muscular atrophy. Sci Transl Med. 2011 Mar 2;3(72):72ra18. doi: 10.1126/scitranslmed.3001777.

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Piper MC, Pinnell LE, Darrah J, Maguire T, Byrne PJ. Construction and validation of the Alberta Infant Motor Scale (AIMS). Can J Public Health. 1992 Jul-Aug;83 Suppl 2:S46-50.

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Porensky PN, Mitrpant C, McGovern VL, Bevan AK, Foust KD, Kaspar BK, Wilton SD, Burghes AH. A single administration of morpholino antisense oligomer rescues spinal muscular atrophy in mouse. Hum Mol Genet. 2012 Apr 1;21(7):1625-38. doi: 10.1093/hmg/ddr600. Epub 2011 Dec 20.

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Rutkove SB, Shefner JM, Gregas M, Butler H, Caracciolo J, Lin C, Fogerson PM, Mongiovi P, Darras BT. Characterizing spinal muscular atrophy with electrical impedance myography. Muscle Nerve. 2010 Dec;42(6):915-21. doi: 10.1002/mus.21784.

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Tiziano FD, Pinto AM, Fiori S, Lomastro R, Messina S, Bruno C, Pini A, Pane M, D'Amico A, Ghezzo A, Bertini E, Mercuri E, Neri G, Brahe C. SMN transcript levels in leukocytes of SMA patients determined by absolute real-time PCR. Eur J Hum Genet. 2010 Jan;18(1):52-8. doi: 10.1038/ejhg.2009.116.

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Valori CF, Ning K, Wyles M, Mead RJ, Grierson AJ, Shaw PJ, Azzouz M. Systemic delivery of scAAV9 expressing SMN prolongs survival in a model of spinal muscular atrophy. Sci Transl Med. 2010 Jun 9;2(35):35ra42. doi: 10.1126/scitranslmed.3000830.

Reference Type BACKGROUND
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Other Identifiers

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U01NS079163

Identifier Type: NIH

Identifier Source: secondary_id

View Link

NN101

Identifier Type: -

Identifier Source: org_study_id

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