Clinical trial NCT01918501: Testing Mitochondria Activity and Blood Lipid Content of Multiple Sclerosis Patients
Official title: Testing Mitochondria Activity and Blood Lipid Content of Multiple Sclerosis Patients
Study type: INTERVENTIONAL
Overall status: UNKNOWN
Phase: NA
Conditions: Multiple Sclerosis
Keywords: multiple sclerosis
Remyelination
Mitochondria
fatty acids
Lead sponsor: Ziv Hospital
Sponsor class: OTHER_GOV
First posted: 2013-08-07
Enrollment: 120
Sex: ALL
Minimum age (years): 18
Maximum age (years): 60
Standard ages: ADULT
Accepts healthy volunteers: yes
Allocation: NA
Intervention model: SINGLE_GROUP
Primary purpose: BASIC_SCIENCE

Brief summary: Background: Multiple sclerosis (MS) is a complex and multifactorial neurological disease characterized by infiltration of immune cells and progressive damage to myelin and axons. Remyelination, the generation of new myelin in the adult nervous system, is an endogenous repair mechanism that restores function of axons. Neurons require considerable energy for their activities, including synaptic neurotransmission, and hence have significant numbers of mitochondria. Unlike other cell types that are able to utilize glycolysis as an alternative energy source, glycolysis in fully differentiated neurons is basically suppressed to maintain their antioxidant status. This property makes neurons highly vulnerable to ATP deficiency, and may be a factor in the susceptibility of neurons to cell death. Mitochondria provide cellular energy by converting oxygen and nutrients into adenosine triphosphate (ATP); and reflect local metabolic needs and via oxidative phosphorylation. Nervous tissues contain about 70% lipids of their dry weight, and around 40% of these lipids are polyunsaturated fatty acids (PUFAs).

Goal: Understanding the relationship between blood composition, mitochondria role and clinical status.

Here, we will examine expression levels of different fatty acids in the blood and monitor mitochondrial transmembrane potential as marker for the mitochondria general function.

Hypothesis: Remyelination efficiency in MS is likely mediated by many factors, besides reducing inflammation. Remyelination may not be achieved correctly /sufficient in MS patients due to nutrition low content causing mitochondrial dysfunction and/or due to fatty acid molecules deficit unable to create a new myelin layer.

Detailed description: Methods: The study will be authorized by the Ziv Helsinki Committee. Informed consent and questionnaire will obtained from all subjects before study entry. We will examine 120 volunteers in a blind fashion, including 60 MS patients diagnosed by a neurologist based on clinical, laboratory and MRI findings. Patients will be evaluated according to EDSS score. The control group will include 50 age and gender matched healthy volunteers and 10 more patients with unrelated neurological diseases. Inclusion criteria: Age 18-60; Exclusion criteria: Other diseases, pathologies, or immune system disorders. Here, we will examine expression of different fatty acids in the serum and in erythrocyte samples; Monitor mitochondrial transmembrane potential as marker for the mitochondria general function.

Eligibility criteria: Inclusion Criteria:

* Age 18-60

Exclusion Criteria:

* Other diseases, pathologies, or immune system disorders.

Primary outcomes:
measure: Levels of approximately 30 fatty acids in the serum and in erythrocyte samples.
timeFrame: Up to 2 years
Secondary outcomes:
measure: Monitor mitochondrial transmembrane potential as a marker for the mitochondria general function.
timeFrame: Up to 2 years
Other outcomes:
measure: Develop a simple method for utilizing common flow cytometry to identify MS by examining the response of lymphocytes to myelin antigens.
timeFrame: Up to 2 years
Locations:
city: Safed
country: Israel
facility: ZIV Medical Center
Study officials:
affiliation: Ziv Medical Center
name: RADI SHAHIEN, MD
role: PRINCIPAL_INVESTIGATOR
References: