Research Topic

Mitochondrial Therapy in Neurological Diseases

About this Research Topic

Mitochondria contain their own DNA and are responsible for supplying more than 90% of energy our body needs. Mitochondrial DNA mutations, such as G11778A (ND4), G3460A (ND1) or T14484C (ND6), results in degeneration of retinal ganglion cells and subsequent bilateral loss of central vision. Mutations of MT-ND1, MT-ND5 and MT-TL1 genes have been implicated in mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Early signs of MELAS include muscle weakness and pain, recurrent headaches, and seizures. Repeated stroke-like episodes often lead to brain damage, vision loss, movement disorder, and dementia. Difficulty of mitochondrial gene-editing has been one of the major bottlenecks in correcting mitochondria-related disorders. In addition, mitochondrial dysfunction accompanies damages to brain and heart (traumatic brain injury, stroke, and heart diseases), of which functions need high level of ATP. To this end, mitochondrial transplantation presents a new paradigm of therapeutic intervention that benefits neuronal survival and regeneration for neurological diseases, including stroke and CNS injury. Supplement of mitochondria to injured brain or nervous system are known to promote neuronal viability, activity and neurite re-growth. The quality of isolated mitochondria and their sources dictate the therapeutic efficacy.

This Research Topic will focus on identification of new mitochondria-related diseases, potential therapy for these diseases and welcomes original research articles and reviews related to clinical evidence of mitochondria-related symptoms, mitochondrial gene-editing, mitochondrial transplantation and mitochondrial cell therapy for neurological diseases.

We welcome authors to address the following topics:
•Evidence of mitochondrial dysfunction in neurological diseases
• Evidence of mitochondrial transplantation in treating neurological diseases
• Mitochondrial gene-editing for neurological disease
• Clinical trials of mitochondrial therapy
• Potential of mitochondrial-enriched cell therapy
•Novel findings on mitochondrial biogenesis in treating neurological diseases


Keywords: Mitochondria, DNA mutations, neurological disease, CNS injury


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Mitochondria contain their own DNA and are responsible for supplying more than 90% of energy our body needs. Mitochondrial DNA mutations, such as G11778A (ND4), G3460A (ND1) or T14484C (ND6), results in degeneration of retinal ganglion cells and subsequent bilateral loss of central vision. Mutations of MT-ND1, MT-ND5 and MT-TL1 genes have been implicated in mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Early signs of MELAS include muscle weakness and pain, recurrent headaches, and seizures. Repeated stroke-like episodes often lead to brain damage, vision loss, movement disorder, and dementia. Difficulty of mitochondrial gene-editing has been one of the major bottlenecks in correcting mitochondria-related disorders. In addition, mitochondrial dysfunction accompanies damages to brain and heart (traumatic brain injury, stroke, and heart diseases), of which functions need high level of ATP. To this end, mitochondrial transplantation presents a new paradigm of therapeutic intervention that benefits neuronal survival and regeneration for neurological diseases, including stroke and CNS injury. Supplement of mitochondria to injured brain or nervous system are known to promote neuronal viability, activity and neurite re-growth. The quality of isolated mitochondria and their sources dictate the therapeutic efficacy.

This Research Topic will focus on identification of new mitochondria-related diseases, potential therapy for these diseases and welcomes original research articles and reviews related to clinical evidence of mitochondria-related symptoms, mitochondrial gene-editing, mitochondrial transplantation and mitochondrial cell therapy for neurological diseases.

We welcome authors to address the following topics:
•Evidence of mitochondrial dysfunction in neurological diseases
• Evidence of mitochondrial transplantation in treating neurological diseases
• Mitochondrial gene-editing for neurological disease
• Clinical trials of mitochondrial therapy
• Potential of mitochondrial-enriched cell therapy
•Novel findings on mitochondrial biogenesis in treating neurological diseases


Keywords: Mitochondria, DNA mutations, neurological disease, CNS injury


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

22 March 2021 Manuscript
25 June 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

22 March 2021 Manuscript
25 June 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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