Testing Mitochondria Activity and Blood Lipid Content of Multiple Scle
Testing Mitochondria Activity and Blood Lipid Content of Multiple Sclerosis Patients
What it found
We found no results in the registry or in papers.
What was tested
Treatment tested
- Blood testing
What it measured
Main measures
Levels of approximately 30 fatty acids in the serum and in erythrocyte samples.
Up to 2 years
Other measures (1)
Monitor mitochondrial transmembrane potential as a marker for the mitochondria general function.
Up to 2 years
Immune response
Who could take part
MS (type not specified) · 18 to 60
Show the full criteria
Inclusion criteria
* Age 18-60
Exclusion criteria
* Other diseases, pathologies, or immune system disorders.
As registered. Criteria can change, so ask the trial team or your neurologist.
About this trial
In the sponsor's words
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.
Loading reviews and guidelines…
History
Started
Aug 2013
Main results due
Jul 2015
Finished
Jul 2015