Research Topic

Molecular Links between Mitochondrial Damage and Parkinson's Disease and Related Disorders

About this Research Topic

Mitochondria is a key organelle to understand the pathogenesis of neurodegenerative disorders such as Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration (FTLD). Increased oxidative stress caused by mitochondrial degeneration has been reported in PD and ALS. The finding that mitochondrial toxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone reproduce the phenotypes in animal models of PD strengthens the involvement of mitochondria in neurodegeneration. Genetic factors responsible for these diseases further revealed that the dysfunction of mitochondrial respiratory activity, the dysregulation of redox status, the defects of mitochondrial quality control are closely linked to the disease etiology.

The early-onset Parkinson’s disease genes PINK1 and Parkin are involved in the mitochondrial quality control by suppression of the motility of damaged mitochondria in the neurons and removal of damaged mitochondria via mitophagy and in the translation regulation of certain nuclear-encoded mitochondrial genes. PD and ALS-FTLD-associated CHCHD2 and CHCHD10 regulate the mitochondrial respiratory activity and cristae organization. The accumulation of α-Synuclein, TDP-43, FUS and SOD1 in and out of mitochondria are pathological features of these diseases. However, due to multifaceted roles of mitochondria in neurons and glial cells, many unsolved questions remain in this research field.

This Research Topic is focused on the pathological role of mitochondria in neurodegenerative disorders including, but are not limited to, PD, ALS and FTDL. Original Research, Reviews, Methods and Opinion articles are welcome.


Keywords: Mitochondrial Transport, Mitochondrial Stress Responses, Mitochondria-Mediated Cell Death, Mitochondria in Glia And Neurons, Molecular Regulation


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 is a key organelle to understand the pathogenesis of neurodegenerative disorders such as Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration (FTLD). Increased oxidative stress caused by mitochondrial degeneration has been reported in PD and ALS. The finding that mitochondrial toxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone reproduce the phenotypes in animal models of PD strengthens the involvement of mitochondria in neurodegeneration. Genetic factors responsible for these diseases further revealed that the dysfunction of mitochondrial respiratory activity, the dysregulation of redox status, the defects of mitochondrial quality control are closely linked to the disease etiology.

The early-onset Parkinson’s disease genes PINK1 and Parkin are involved in the mitochondrial quality control by suppression of the motility of damaged mitochondria in the neurons and removal of damaged mitochondria via mitophagy and in the translation regulation of certain nuclear-encoded mitochondrial genes. PD and ALS-FTLD-associated CHCHD2 and CHCHD10 regulate the mitochondrial respiratory activity and cristae organization. The accumulation of α-Synuclein, TDP-43, FUS and SOD1 in and out of mitochondria are pathological features of these diseases. However, due to multifaceted roles of mitochondria in neurons and glial cells, many unsolved questions remain in this research field.

This Research Topic is focused on the pathological role of mitochondria in neurodegenerative disorders including, but are not limited to, PD, ALS and FTDL. Original Research, Reviews, Methods and Opinion articles are welcome.


Keywords: Mitochondrial Transport, Mitochondrial Stress Responses, Mitochondria-Mediated Cell Death, Mitochondria in Glia And Neurons, Molecular Regulation


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

02 August 2020 Manuscript

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

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Topic Editors

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Submission Deadlines

02 August 2020 Manuscript

Participating Journals

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

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