Mitochondrial dna in ms

A forum to discuss research on the origins of MS and its development.

Mitochondrial dna in ms

Postby frodo » Sat Dec 16, 2017 6:11 am

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Re: Mitochondrial dna in ms

Postby NHE » Sat Dec 16, 2017 7:14 am

Mitochondrial DNA (mtDNA) can act as damage-associated molecular pattern molecule (DAMP) and initiate an inflammatory response. We hypothesized that the concentration of mtDNA might reflect inflammatory activity in multiple sclerosis and investigated therefore levels of cell-free mitochondrial DNA in cerebrospinal fluid of patients with relapsing-remitting multiple sclerosis. Significantly higher levels of mtDNA were found in patients compared to controls and there was an inverse correlation between disease duration and mtDNA concentration. Our study suggests that mitochondria can be involved early in multiple sclerosis, but whether this is as an initiator of the inflammatory response or part of its maintenance is unclear. Further, our study suggests that changes in mtDNA may provide a novel marker for early disease activity.

Perhaps the mtDNA is evidence that MS is a neurodegenerative disease with loss of mitochondria as an early step in its etiology.
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Re: Mitochondrial dna in ms

Postby frodo » Tue Jan 09, 2018 12:14 pm

NHE wrote:Perhaps the mtDNA is evidence that MS is a neurodegenerative disease with loss of mitochondria as an early step in its etiology.


There are recent news in the mitochondria front. Look at this.

Insights in pathogenesis of multiple sclerosis: nitric oxide may induce mitochondrial dysfunction of oligodendrocytes

https://www.degruyter.com/view/j/revneu ... 7-0033.xml

Abstract

Demyelinating diseases, such as multiple sclerosis (MS), are kinds of common diseases in the central nervous system (CNS), and originated from myelin loss and axonal damage.

Oligodendrocyte dysfunction is the direct reason of demyelinating lesions in the CNS. Nitric oxide (NO) plays an important role in the pathological process of demyelinating diseases. Although the neurotoxicity of NO is more likely mediated by peroxynitrite rather than NO itself, NO can impair oligodendrocyte energy metabolism through mediating the damaging of mitochondrial DNA, mitochondrial membrane and mitochondrial respiratory chain complexes.

In the progression of MS, NO can mainly mediate demyelination, axonal degeneration and cell death. Hence, in this review, we extensively discuss endangerments of NO in oligodendrocytes (OLs), which is suggested to be the main mediator in demyelinating diseases, e.g. MS.

We hypothesize that NO takes part in MS through impairing the function of monocarboxylate transporter 1, especially causing axonal degeneration. Then, it further provides a new insight that NO for OLs may be a reliable therapeutic target to ameliorate the course of demyelinating diseases.
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