About this Research Topic
Neurons predominantly rely on high quality mitochondria to provide the necessary energy demands required to maintain essential neuronal functions including neuronal connectivity, neuronal activity, neuronal development and survival. Importantly, high quality mitochondria are necessary to provide the necessary energy and a low level of oxidative stress to maintain proper executive functions including self-regulation, working memory, focus and planning skills in humans. In order for neurons to maintain a level of high-quality mitochondria, mitochondria must undergo constant fission and fusion, be able to efficiently buffer calcium, traffic to sites of high-energy demands including dendrites and axons, and continuously undergo turnover (mitophagy) and biogenesis.
On the other hand, mitochondrial dysfunction- caused by an overt accumulation of mitochondrial DNA mutations, altered calcium levels, and mitochondrial-derived reactive oxygen species- contributes to age-related cognitive decline and underlies the etiology of many age-related neurodegenerative disorders including Parkinson’s disease, Lewy Body dementia and Alzheimer’s disease. Mitochondrial dysfunction is defined by a progressive decrease in mitochondrial-derived ATP, a lack of mitochondrial mobility (trafficking) to distal sites of dendrites and axons, a decrease in transmembrane potential leading to inefficiently coupled mitochondria, overtly fragmented mitochondria and an inability to handle cytosolic calcium. However, how normal brain aging leads to mitochondrial dysfunction and the pathological mechanisms by which mitochondrial dysfunction contribute to neurodegeneration and cognitive decline in age-related neurodegenerative disease are beginning to be elucidated.
For this Research Topic, we welcome the submission of original and high quality research manuscripts and reviews that focus on the interplay that altered bioenergetics, oxidative stress, mitochondrial dysfunction and altered mitochondrial calcium handling contribute to the pathogenesis of age-related cognitive decline and neurodegenerative diseases. Reviews that focus on recent advances in the development of “mito-protective therapies” to reverse mitochondrial dysfunction and neurodegeneration are also welcome.
On the other hand, mitochondrial dysfunction- caused by an overt accumulation of mitochondrial DNA mutations, altered calcium levels, and mitochondrial-derived reactive oxygen species- contributes to age-related cognitive decline and underlies the etiology of many age-related neurodegenerative disorders including Parkinson’s disease, Lewy Body dementia and Alzheimer’s disease. Mitochondrial dysfunction is defined by a progressive decrease in mitochondrial-derived ATP, a lack of mitochondrial mobility (trafficking) to distal sites of dendrites and axons, a decrease in transmembrane potential leading to inefficiently coupled mitochondria, overtly fragmented mitochondria and an inability to handle cytosolic calcium. However, how normal brain aging leads to mitochondrial dysfunction and the pathological mechanisms by which mitochondrial dysfunction contribute to neurodegeneration and cognitive decline in age-related neurodegenerative disease are beginning to be elucidated.
For this Research Topic, we welcome the submission of original and high quality research manuscripts and reviews that focus on the interplay that altered bioenergetics, oxidative stress, mitochondrial dysfunction and altered mitochondrial calcium handling contribute to the pathogenesis of age-related cognitive decline and neurodegenerative diseases. Reviews that focus on recent advances in the development of “mito-protective therapies” to reverse mitochondrial dysfunction and neurodegeneration are also welcome.
Keywords: mitochondrial dynamics, mitochondrial import, mitochondrial biogenesis, calcium signaling, mitophagy, mitochondrial trafficking, bioenergetics, oxidative stress, neurotrophic signalling, neurodegeneration
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