The MURDOCK Study Community Registry and Biorepository Multiple Sclerosis Cohort
Status: | Active, not recruiting |
---|---|
Conditions: | Neurology, Multiple Sclerosis |
Therapuetic Areas: | Neurology, Other |
Healthy: | No |
Age Range: | 18 - Any |
Updated: | 12/14/2016 |
Start Date: | June 2010 |
End Date: | August 2017 |
The goal of this study is to enroll 1000 participants with a history of Multiple Sclerosis
into the MURDOCK Study (Duke IRB Pro00011196) as well as into the Multiple Sclerosis Cohort
study (Duke IRB Pro00023791). All 1000 participants will answer a 4-page questionnaire
administered by a trained study coordinator which is designed to collect information on the
participant's diagnosis of Multiple Sclerosis. The goal of the study is to seek genetic
explanations for response to treatment, progression of the disease, and biomarker
validation.
into the MURDOCK Study (Duke IRB Pro00011196) as well as into the Multiple Sclerosis Cohort
study (Duke IRB Pro00023791). All 1000 participants will answer a 4-page questionnaire
administered by a trained study coordinator which is designed to collect information on the
participant's diagnosis of Multiple Sclerosis. The goal of the study is to seek genetic
explanations for response to treatment, progression of the disease, and biomarker
validation.
Despite tremendous research efforts, the targets of immune response and the mechanisms for
neuronal loss associated with MS have not been fully characterized. Although substantial
advances have been made in the development of therapeutic treatments, the drugs currently
available to MS patients do not significantly alter the long-term prognosis of the disease.
Better markers that represent the biological activity of the disease process and response to
therapy are desperately needed. MS is thought to be mediated by autoimmunity which causes
demyelination and transection of axons throughout the brain and spinal cord resulting in the
formation of multiple scars (or scleroses) on axon myelin sheaths and reducing electrical
conductivity and decreased CNS signaling. It is most common in young adults; more than 90%
of patients are diagnosed before the age of 55 and less than 5% before the age of 14.
Females are 2-3 times more frequently affected than males and children of affected females
are at a significantly higher risk of developing MS than children of affected males. A
strong genetic component is suggested by the co-occurrence of cases within families and the
high disease prevalence in some ethnic populations (particularly those of northern European
origin) compared with others (African and Asian groups) irrespective of geographic
location.7 The incidence of MS in northern Europe, where the genetically associated
haplotype HLA DR2 is most common, is as high as 1 per 750 individuals. MS affects more than
400,000 people in the U.S. and 2.5 million worldwide.
Although numerous putative MS-specific biomarkers, representing different mechanisms of
pathogenesis and steps along the inflammatory cascade have been proposed, none have been
fully validated. To date, the majority of studies identifying biomarkers associated with MS
initiation or progression have been limited to investigation of one to several markers at a
time; only one study has attempted open platform proteomic profiling in MS; however, the
study size was relatively small and the clinical homogeneity of the dataset of the study is
not clear. To understand a complex disease like MS, high throughput technologies capable of
profiling multiple etiological changes is needed as well as a well-define population of
those with the disease.
neuronal loss associated with MS have not been fully characterized. Although substantial
advances have been made in the development of therapeutic treatments, the drugs currently
available to MS patients do not significantly alter the long-term prognosis of the disease.
Better markers that represent the biological activity of the disease process and response to
therapy are desperately needed. MS is thought to be mediated by autoimmunity which causes
demyelination and transection of axons throughout the brain and spinal cord resulting in the
formation of multiple scars (or scleroses) on axon myelin sheaths and reducing electrical
conductivity and decreased CNS signaling. It is most common in young adults; more than 90%
of patients are diagnosed before the age of 55 and less than 5% before the age of 14.
Females are 2-3 times more frequently affected than males and children of affected females
are at a significantly higher risk of developing MS than children of affected males. A
strong genetic component is suggested by the co-occurrence of cases within families and the
high disease prevalence in some ethnic populations (particularly those of northern European
origin) compared with others (African and Asian groups) irrespective of geographic
location.7 The incidence of MS in northern Europe, where the genetically associated
haplotype HLA DR2 is most common, is as high as 1 per 750 individuals. MS affects more than
400,000 people in the U.S. and 2.5 million worldwide.
Although numerous putative MS-specific biomarkers, representing different mechanisms of
pathogenesis and steps along the inflammatory cascade have been proposed, none have been
fully validated. To date, the majority of studies identifying biomarkers associated with MS
initiation or progression have been limited to investigation of one to several markers at a
time; only one study has attempted open platform proteomic profiling in MS; however, the
study size was relatively small and the clinical homogeneity of the dataset of the study is
not clear. To understand a complex disease like MS, high throughput technologies capable of
profiling multiple etiological changes is needed as well as a well-define population of
those with the disease.
Inclusion Criteria:
- 18 years of age or older
- Multiple Sclerosis Diagnosis or self report Multiple Sclerosis
Exclusion Criteria:
- Participants who are not willing to participate in this study
We found this trial at
5
sites
Raleigh, North Carolina 27607
Principal Investigator: Simon Gregory, PhD
Phone: 919-719-8826
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Concord, North Carolina 28205
Principal Investigator: Simon Gregory, PhD
Phone: 704-250-5861
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Davidson, North Carolina 28036
Principal Investigator: Simon Gregory, PhD
Phone: 704-250-5861
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Durham, North Carolina 27705
Principal Investigator: Simon Gregory, PhD
Phone: 919-695-6413
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Kannapolis, North Carolina 28081
Principal Investigator: Simon Gregory, PhD
Phone: 704-250-5861
Click here to add this to my saved trials