Neurons are characterized by a long lifespan and large energy requirements, which is necessary for their elevated transcriptional and translational activity, synthesis of organelles, neurotransmission and maintenance of the redox homeostasis. For this reason, neurons are very sensitive to stressors leading to energy imbalance. Impaired energy homeostasis is implicated in neuronal dysfunction. Mitochondria possess their own DNA (mtDNA) and are essential for the regulation of key cellular processes such as energy metabolism, the response to oxidative stress, and cellular pathways modulating cell death or survival. Mitochondria produce ATP, which is indispensable for neuronal function and regeneration. Neurons show highly polarized structures and need to deliver mitochondria throughout long axons and terminal branches, where there is specific high energy demand. Mitochondria play also a key role in calcium buffering at synapses. Mitochondria fusion/fission dynamic and mitochondria transcellular transfer are implicated in the maintenance of neuronal function.
Chronic mitochondrial alterations together with bioenergetic failure are pathological hallmarks of neurodegenerative diseases. The multitude of functions played by mitochondria requires a rigid modulation of protein dynamics and turnover. Several pathways, frequently overlapping, are implicated in this regulation. The progression of several neurodegenerative diseases is associated with alterations in these regulatory pathways. Recent studies are demonstrating that disease-associated proteins directly affect mitochondria homeostasis and function. Chronic inflammation is also a hallmark of neurodegenerative diseases. Recent data are suggesting that mitochondria can activate the pro-inflammatory cascade, although the molecular mechanisms implicated are not yet fully elucidated. Notably, several neurodegenerative diseases show energy imbalance and altered glucose homeostasis, suggesting a tight inter-correlation between mitochondrial function, energy homeostasis, inflammation and neurodegeneration. However, the understanding of the link between energy homeostasis and neurodegeneration is not yet fully investigated. We would like to get deeper into this field by providing new molecular pathways that underline the link between mitochondria-mediated regulation of energy homeostasis and neuronal function.
The scope of this research topic is to underline and discuss the intrinsic mechanisms that neurons employ to maintain or reprogram axonal mitochondrial density and integrity, and their bioenergetic capacity, upon sensing energy stress. We encourage the submission of articles that address the most recent advances in unveiling the molecular pathways that affect the mitochondrial function in regulating the energy homeostasis and their link with the signaling cascade leading to neurodegeneration. We are also interested in articles describing potential therapeutic strategies that target bioenergetic restoration to power neuronal survival, function, and regeneration.
Original articles are the main focus of this Topic, but also review articles providing overviews of new insight are also welcome.
Neurons are characterized by a long lifespan and large energy requirements, which is necessary for their elevated transcriptional and translational activity, synthesis of organelles, neurotransmission and maintenance of the redox homeostasis. For this reason, neurons are very sensitive to stressors leading to energy imbalance. Impaired energy homeostasis is implicated in neuronal dysfunction. Mitochondria possess their own DNA (mtDNA) and are essential for the regulation of key cellular processes such as energy metabolism, the response to oxidative stress, and cellular pathways modulating cell death or survival. Mitochondria produce ATP, which is indispensable for neuronal function and regeneration. Neurons show highly polarized structures and need to deliver mitochondria throughout long axons and terminal branches, where there is specific high energy demand. Mitochondria play also a key role in calcium buffering at synapses. Mitochondria fusion/fission dynamic and mitochondria transcellular transfer are implicated in the maintenance of neuronal function.
Chronic mitochondrial alterations together with bioenergetic failure are pathological hallmarks of neurodegenerative diseases. The multitude of functions played by mitochondria requires a rigid modulation of protein dynamics and turnover. Several pathways, frequently overlapping, are implicated in this regulation. The progression of several neurodegenerative diseases is associated with alterations in these regulatory pathways. Recent studies are demonstrating that disease-associated proteins directly affect mitochondria homeostasis and function. Chronic inflammation is also a hallmark of neurodegenerative diseases. Recent data are suggesting that mitochondria can activate the pro-inflammatory cascade, although the molecular mechanisms implicated are not yet fully elucidated. Notably, several neurodegenerative diseases show energy imbalance and altered glucose homeostasis, suggesting a tight inter-correlation between mitochondrial function, energy homeostasis, inflammation and neurodegeneration. However, the understanding of the link between energy homeostasis and neurodegeneration is not yet fully investigated. We would like to get deeper into this field by providing new molecular pathways that underline the link between mitochondria-mediated regulation of energy homeostasis and neuronal function.
The scope of this research topic is to underline and discuss the intrinsic mechanisms that neurons employ to maintain or reprogram axonal mitochondrial density and integrity, and their bioenergetic capacity, upon sensing energy stress. We encourage the submission of articles that address the most recent advances in unveiling the molecular pathways that affect the mitochondrial function in regulating the energy homeostasis and their link with the signaling cascade leading to neurodegeneration. We are also interested in articles describing potential therapeutic strategies that target bioenergetic restoration to power neuronal survival, function, and regeneration.
Original articles are the main focus of this Topic, but also review articles providing overviews of new insight are also welcome.
