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Manuscript Submission Deadline 31 May 2023

Mitochondria are essential cytoplasmic organelles regulating numerous cellular processes, like ATP production, calcium storage, and cell death. At neuronal level, mitochondria are involved in neurogenesis, neuronal survival, synaptic transmission and plasticity, among others. Therefore, neuronal cells critically depend on mitochondrial functions to fulfill and maintain their physiological activity. The homeostasis of these cytoplasmic organelles is preserved by maintaining a perfect balance between fusion and fission, biogenesis and mitophagy, bidirectional trafficking from soma to neuronal synapses and vice versa, and other important mitochondrial processes. The dysfunction of a single mitochondrial mechanism could jeopardize the entire cell physiology, thus leading to the onset of complex human diseases.

Given their fundamental role in supporting neuronal functions, it is not surprising that countless studies have linked mitochondrial damage with the onset and progression of neuro-degenerative, -psychiatric, and -developmental disorders. Despite great progress has been made in deciphering the pathological pathways impacting neuronal function and survival, the pharmacological therapies currently prescribed for the majority of these brain disorders can treat just the symptoms, but not the actual cause of the disease. This unsolved issue necessitates the use of advanced multi-omics, systems biology, and artificial intelligence approaches to mechanistically understand the molecular etiologies and accelerate the therapeutic development for these complex neuronal diseases.

The goal of this Research Topic is to achieve a better understating of the impact of mitochondrial damage on the onset of neuro-degenerative, -psychiatric, and -developmental disorders in order to pinpoint possible molecular targets for medical intervention.

The scope of this Research Topic covers the following:
• Mitochondrial dysfunctions in neuro-degenerative, -psychiatric, and -developmental disorders;
• Mitochondrial damage repercussion on neuronal activity;
• Mitochondrial impairment and its association with neuroinflammation and immune response;
• Pharmacological treatments used in neuro-degenerative, -psychiatric, and -developmental disorders and their impact on mitochondrial function;
• Data-driven and experimental approaches for the identification of repurposable drug candidates (i.e., drug repurposing);
• Systems biology and artificial intelligence approaches for deciphering or predicting mitochondrial and neuronal damage in brain disorders.

All types of manuscripts are welcome.

Keywords: Neurodegeneration, Neuropsychiatry, Neurodevelopmental disorders, Mitochondria, Pharmacological treatments, Omics, Systems Biology


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 are essential cytoplasmic organelles regulating numerous cellular processes, like ATP production, calcium storage, and cell death. At neuronal level, mitochondria are involved in neurogenesis, neuronal survival, synaptic transmission and plasticity, among others. Therefore, neuronal cells critically depend on mitochondrial functions to fulfill and maintain their physiological activity. The homeostasis of these cytoplasmic organelles is preserved by maintaining a perfect balance between fusion and fission, biogenesis and mitophagy, bidirectional trafficking from soma to neuronal synapses and vice versa, and other important mitochondrial processes. The dysfunction of a single mitochondrial mechanism could jeopardize the entire cell physiology, thus leading to the onset of complex human diseases.

Given their fundamental role in supporting neuronal functions, it is not surprising that countless studies have linked mitochondrial damage with the onset and progression of neuro-degenerative, -psychiatric, and -developmental disorders. Despite great progress has been made in deciphering the pathological pathways impacting neuronal function and survival, the pharmacological therapies currently prescribed for the majority of these brain disorders can treat just the symptoms, but not the actual cause of the disease. This unsolved issue necessitates the use of advanced multi-omics, systems biology, and artificial intelligence approaches to mechanistically understand the molecular etiologies and accelerate the therapeutic development for these complex neuronal diseases.

The goal of this Research Topic is to achieve a better understating of the impact of mitochondrial damage on the onset of neuro-degenerative, -psychiatric, and -developmental disorders in order to pinpoint possible molecular targets for medical intervention.

The scope of this Research Topic covers the following:
• Mitochondrial dysfunctions in neuro-degenerative, -psychiatric, and -developmental disorders;
• Mitochondrial damage repercussion on neuronal activity;
• Mitochondrial impairment and its association with neuroinflammation and immune response;
• Pharmacological treatments used in neuro-degenerative, -psychiatric, and -developmental disorders and their impact on mitochondrial function;
• Data-driven and experimental approaches for the identification of repurposable drug candidates (i.e., drug repurposing);
• Systems biology and artificial intelligence approaches for deciphering or predicting mitochondrial and neuronal damage in brain disorders.

All types of manuscripts are welcome.

Keywords: Neurodegeneration, Neuropsychiatry, Neurodevelopmental disorders, Mitochondria, Pharmacological treatments, Omics, Systems Biology


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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