alexa Mitochondrial DNA Mutation in Microglia Can Be Treated
ISSN: 2376-0389

Journal of Multiple Sclerosis
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Review Article

Mitochondrial DNA Mutation in Microglia Can Be Treated by SCNT Cloning and Not by Reprogramming of Olfactory Ensheathing Cells in the Multiple Sclerosis Treatment

Abdul Mannan Baig*

Department of Biological and Biomedical Sciences, Aga Khan University, Karachi, Pakistan

Corresponding Author:
Abdul Mannan Baig
Department of Biological and Biomedical Sciences
Aga Khan University, Stadium Road, Karachi, Pakistan
Tel: 92-(0)21-3486-4435
Fax: 92-(0)21-3493-4294
E-mail: [email protected]

Received date: October 20, 2014; Accepted date: November 11, 2014; Published date: November 14, 2014

Citation: Baig AM (2015) Mitochondrial DNA Mutation in Microglia Can Be Treated by SCNT Cloning and Not by Reprogramming of Olfactory Ensheathing Cells in the Multiple Sclerosis Treatment. J Mult Scler 2:132. doi:10.4172/2376-0389.1000132

Copyright: ©2014 Baig AM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Background: Multiple sclerosis (MS) is a demyelinating chronic inflammatory neurological disease of the central nervous system (CNS), characterized by activation of microglia. Mitochondrial mutations (mtDNA.mutat) and dysfunctions in microglial cells are thought to centrally contribute to the damaging effects of neuroinflammation seen in MS.
Objective: The somatic nuclear transfer (SCNT) technology offers a more practical mode of therapy in MS, This method would attempt to dilute and/or progressively replace the (mtDNA.mutat) and activated microglia with cloned olfactory ensheathing cells (OEC) with remyelinating and scavenging properties which would attempt to limit the progression of MS.
Proposed Methods: Applying SCNT-derived embryonic stem (ES) cells based therapy by cloning olfactory ensheathing cells (OEC), engineered with an autologous nuclear component of the recipient OEC with a healthy donor oocyte. The inner cell mass of the subsequently developed blastocyst would be the source to generate the microglia. The novel proposed transcribrial route device offers a painless mode of cell transplantation to the brain.
Expected Results: This mode of generating SCNT cloned glia and its transplantation to the brain is expected to replace the (mtDNA.mutat) and activated microglia of the patients with MS and use the regenerative and remyelinating and properties of the OEC’s, as has been seen in recent clinical trials in paraplegic patients with spinal cord injuries.
Conclusion: The use of SCNT in contrast to the reprogramming adult somatic cell is expected to develop isogenic ES cell-based therapies for the prevention and treatment of MS associated with mtDNA mutations that may open a new avenue of designer’s targeted cell therapy unique for the patients with MS. The proposed “transcribrial device” to access the brain can be an advantageous route of delivery of cloned cells to the brain.

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