Mitochondria are high dynamic organelles, which provide ATP, calcium buffering, ROS, etc., to regulate cell development, metabolism, and cellular signaling. Various processes such as movement, fusion, fission, mitophagy, biogenesis, and proteostasis act as mitochondrial quality control mechanisms.
In the nerve system, mitochondria are vital for neuron growth, synaptic activity, neuroplasticity, and cell viability. Regarding the unique morphological features and great capability to interact with other cell compartments, neuron axons face unique challenges in coordinating mitochondria function with synaptic plasticity and mitochondria health. The axonopathy associated with dysregulated and dysfunctional mitochondria becomes a critical component of many cognitive and degenerative diseases. In dendrites, many physiology and pathology conditions induce translocation of mitochondria into dendritic spines and the areas where high metabolic demand is required. The postsynaptic activity also regulates mitochondrial fission and fusion. Despite the well-recognized regulation of mitochondrial fission/fusion by synaptic activity, the significance of these processes to neural plasticity and brain disorders has yet to be fully elucidated.
Beyond the neuron-centric view, it is also critical to consider the common and unique aspects of mitochondrial biology in the glial cell. Mitochondrial defects and compensatory changes in glial cells are detrimental to neurons.
Earlier reports have implicated a possible linkage between aberrant mitochondrial quality control and some neurodegenerative, neurodevelopmental, and psychiatric diseases(i.e., Alzheimer's Disease, Parkinson's Disease, Rett Syndrome, Autism Spectrum Disorders, schizophrenia, bipolar disorder, depression, etc.). Mitochondrial pathology including alterations in mitochondrial morphology, density, number, trafficking, dynamics, distribution, and mitophagy has been observed in some patients' brains or disease-related animal models. For example, PINK1/Parkin-dependent mitophagy in PD, alterations in mitochondrial trafficking in neurons have been reported in Hd mouse brain, and aberrant mitochondrial dynamics machinery has been reported in HD, AD and PD patients, as well as in schizophrenia, MDD and anxiety mouse models. Additionally, a certain number of the mitochondrial genome and nuclear-encoded mitochondrial genes have been suggested repeatedly to be implicated in those diseases. Aiming to manage and/or treat these diseases, several drugs or techniques have been developed to improve or modulate mitochondrial functions in the brain.
Although substantial progress has been made in illustrating how the mitochondria are involved in some neurodegenerative, neurodevelopmental, and psychiatric diseases, a greater understanding of the mechanism through the consequences of mitochondrial defects and mitochondrial quality control system may provide further translational insights and new therapeutic perspectives.
In this Research Topic, we aim to collect Original Research, Review, and Clinical research related to the mitochondrial quality control pathways in neuroplasticity and brain disorders. Potential topics of interest include but are not limited to the following:
1. Novel technologies to study or manipulate mitochondrial quality control pathways in the nerve system.
2. Molecular basis of mitochondrial movement, fusion, fission, mitophagy, biogenesis, and proteostasis in neurons or glial cells.
3. Mitochondrial quality control in neuronal axon and dendrite, metabolic reprogramming, cell-cell metabolic cooperation, redox homeostasis control.
4. Crosstalk between mitochondrial quality control and neuroplasticity machinery.
5. Aberrant Mitochondrial quality control in neurodegenerative, neurodevelopmental, and psychiatric diseases.
6. Regulation of Mitochondrial quality control by neuropsychiatric disease risk factors.
7. The functional role of mitochondria in glial cells and its implications for neuronal survival and brain function, including metabolism, redox homeostasis, Ca2+ signaling, inflammation, and cell death.
Mitochondria are high dynamic organelles, which provide ATP, calcium buffering, ROS, etc., to regulate cell development, metabolism, and cellular signaling. Various processes such as movement, fusion, fission, mitophagy, biogenesis, and proteostasis act as mitochondrial quality control mechanisms.
In the nerve system, mitochondria are vital for neuron growth, synaptic activity, neuroplasticity, and cell viability. Regarding the unique morphological features and great capability to interact with other cell compartments, neuron axons face unique challenges in coordinating mitochondria function with synaptic plasticity and mitochondria health. The axonopathy associated with dysregulated and dysfunctional mitochondria becomes a critical component of many cognitive and degenerative diseases. In dendrites, many physiology and pathology conditions induce translocation of mitochondria into dendritic spines and the areas where high metabolic demand is required. The postsynaptic activity also regulates mitochondrial fission and fusion. Despite the well-recognized regulation of mitochondrial fission/fusion by synaptic activity, the significance of these processes to neural plasticity and brain disorders has yet to be fully elucidated.
Beyond the neuron-centric view, it is also critical to consider the common and unique aspects of mitochondrial biology in the glial cell. Mitochondrial defects and compensatory changes in glial cells are detrimental to neurons.
Earlier reports have implicated a possible linkage between aberrant mitochondrial quality control and some neurodegenerative, neurodevelopmental, and psychiatric diseases(i.e., Alzheimer's Disease, Parkinson's Disease, Rett Syndrome, Autism Spectrum Disorders, schizophrenia, bipolar disorder, depression, etc.). Mitochondrial pathology including alterations in mitochondrial morphology, density, number, trafficking, dynamics, distribution, and mitophagy has been observed in some patients' brains or disease-related animal models. For example, PINK1/Parkin-dependent mitophagy in PD, alterations in mitochondrial trafficking in neurons have been reported in Hd mouse brain, and aberrant mitochondrial dynamics machinery has been reported in HD, AD and PD patients, as well as in schizophrenia, MDD and anxiety mouse models. Additionally, a certain number of the mitochondrial genome and nuclear-encoded mitochondrial genes have been suggested repeatedly to be implicated in those diseases. Aiming to manage and/or treat these diseases, several drugs or techniques have been developed to improve or modulate mitochondrial functions in the brain.
Although substantial progress has been made in illustrating how the mitochondria are involved in some neurodegenerative, neurodevelopmental, and psychiatric diseases, a greater understanding of the mechanism through the consequences of mitochondrial defects and mitochondrial quality control system may provide further translational insights and new therapeutic perspectives.
In this Research Topic, we aim to collect Original Research, Review, and Clinical research related to the mitochondrial quality control pathways in neuroplasticity and brain disorders. Potential topics of interest include but are not limited to the following:
1. Novel technologies to study or manipulate mitochondrial quality control pathways in the nerve system.
2. Molecular basis of mitochondrial movement, fusion, fission, mitophagy, biogenesis, and proteostasis in neurons or glial cells.
3. Mitochondrial quality control in neuronal axon and dendrite, metabolic reprogramming, cell-cell metabolic cooperation, redox homeostasis control.
4. Crosstalk between mitochondrial quality control and neuroplasticity machinery.
5. Aberrant Mitochondrial quality control in neurodegenerative, neurodevelopmental, and psychiatric diseases.
6. Regulation of Mitochondrial quality control by neuropsychiatric disease risk factors.
7. The functional role of mitochondria in glial cells and its implications for neuronal survival and brain function, including metabolism, redox homeostasis, Ca2+ signaling, inflammation, and cell death.
