Mitochondria, energy, and metabolism in neuronal health and disease

Mitochondria are associated with various cellular activities critical to homeostasis, particularly in the nervous system. The plastic architecture of the mitochondrial network and its dynamic structure play crucial roles in ensuring that varying energetic demands are rapidly met to maintain neuronal...

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Published inFEBS letters Vol. 596; no. 9; pp. 1095 - 1110
Main Authors Trigo, Diogo, Avelar, Catarina, Fernandes, Miguel, Sá, Juliana, Cruz e Silva, Odete
Format Journal Article
LanguageEnglish
Published England 01.05.2022
Subjects
ageing
Alzheimer
axon
brain
cognitive disorders
energy
homeostasis
Huntington
metabolism
mitochondria
mitophagy
neurodegeneration
neurodegenerative diseases
neuron
neurons
neuropathology
oxidative stress
Parkinson
ROS
stress response
therapeutics
ageing
mitophagy
mitochondria
ROS
neurodegeneration
neuron
Huntington
axon
Alzheimer
Parkinson
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Abstract Mitochondria are associated with various cellular activities critical to homeostasis, particularly in the nervous system. The plastic architecture of the mitochondrial network and its dynamic structure play crucial roles in ensuring that varying energetic demands are rapidly met to maintain neuronal and axonal energy homeostasis. Recent evidence associates aging and neurodegeneration with anomalous neuronal metabolism as age‐dependent alterations of neuronal metabolism are now believed to occur prior to neurodegeneration. The brain has a high energy demand, which makes it particularly sensitive to mitochondrial dysfunction. Distinct cellular events causing oxidative stress or disruption of metabolism and mitochondrial homeostasis can trigger a neuropathology. This review explores the bioenergetic hypothesis for the neurodegenerative pathomechanisms, discussing factors leading to age‐related brain hypometabolism and its contribution to cognitive decline. Recent research on the mitochondrial network in healthy nervous system cells, its response to stress, and how it is affected by pathology, as well as current contributions to novel therapeutic approaches will be highlighted. This review discusses the hypothesis that hypometabolism and mitochondrial dysfunction in neuronal cells represent pathogenic events triggering cognitive decline and neurodegenerative diseases.
AbstractList Mitochondria are associated with various cellular activities critical to homeostasis, particularly in the nervous system. The plastic architecture of the mitochondrial network and its dynamic structure play crucial roles in ensuring that varying energetic demands are rapidly met to maintain neuronal and axonal energy homeostasis. Recent evidence associates aging and neurodegeneration with anomalous neuronal metabolism as age-dependent alterations of neuronal metabolism are now believed to occur prior to neurodegeneration. The brain has a high energy demand, which makes it particularly sensitive to mitochondrial dysfunction. Distinct cellular events causing oxidative stress or disruption of metabolism and mitochondrial homeostasis can trigger a neuropathology. This review explores the bioenergetic hypothesis for the neurodegenerative pathomechanisms, discussing factors leading to age-related brain hypometabolism and its contribution to cognitive decline. Recent research on the mitochondrial network in healthy nervous system cells, its response to stress, and how it is affected by pathology, as well as current contributions to novel therapeutic approaches will be highlighted.
Mitochondria are associated with various cellular activities critical to homeostasis, particularly in the nervous system. The plastic architecture of the mitochondrial network and its dynamic structure play crucial roles in ensuring that varying energetic demands are rapidly met to maintain neuronal and axonal energy homeostasis. Recent evidence associates aging and neurodegeneration with anomalous neuronal metabolism as age-dependent alterations of neuronal metabolism are now believed to occur prior to neurodegeneration. The brain has a high energy demand, which makes it particularly sensitive to mitochondrial dysfunction. Distinct cellular events causing oxidative stress or disruption of metabolism and mitochondrial homeostasis can trigger a neuropathology. This review explores the bioenergetic hypothesis for the neurodegenerative pathomechanisms, discussing factors leading to age-related brain hypometabolism and its contribution to cognitive decline. Recent research on the mitochondrial network in healthy nervous system cells, its response to stress, and how it is affected by pathology, as well as current contributions to novel therapeutic approaches will be highlighted.Mitochondria are associated with various cellular activities critical to homeostasis, particularly in the nervous system. The plastic architecture of the mitochondrial network and its dynamic structure play crucial roles in ensuring that varying energetic demands are rapidly met to maintain neuronal and axonal energy homeostasis. Recent evidence associates aging and neurodegeneration with anomalous neuronal metabolism as age-dependent alterations of neuronal metabolism are now believed to occur prior to neurodegeneration. The brain has a high energy demand, which makes it particularly sensitive to mitochondrial dysfunction. Distinct cellular events causing oxidative stress or disruption of metabolism and mitochondrial homeostasis can trigger a neuropathology. This review explores the bioenergetic hypothesis for the neurodegenerative pathomechanisms, discussing factors leading to age-related brain hypometabolism and its contribution to cognitive decline. Recent research on the mitochondrial network in healthy nervous system cells, its response to stress, and how it is affected by pathology, as well as current contributions to novel therapeutic approaches will be highlighted.
Mitochondria are associated with various cellular activities critical to homeostasis, particularly in the nervous system. The plastic architecture of the mitochondrial network and its dynamic structure play crucial roles in ensuring that varying energetic demands are rapidly met to maintain neuronal and axonal energy homeostasis. Recent evidence associates aging and neurodegeneration with anomalous neuronal metabolism as age‐dependent alterations of neuronal metabolism are now believed to occur prior to neurodegeneration. The brain has a high energy demand, which makes it particularly sensitive to mitochondrial dysfunction. Distinct cellular events causing oxidative stress or disruption of metabolism and mitochondrial homeostasis can trigger a neuropathology. This review explores the bioenergetic hypothesis for the neurodegenerative pathomechanisms, discussing factors leading to age‐related brain hypometabolism and its contribution to cognitive decline. Recent research on the mitochondrial network in healthy nervous system cells, its response to stress, and how it is affected by pathology, as well as current contributions to novel therapeutic approaches will be highlighted. This review discusses the hypothesis that hypometabolism and mitochondrial dysfunction in neuronal cells represent pathogenic events triggering cognitive decline and neurodegenerative diseases.
Author Sá, Juliana
Trigo, Diogo
Cruz e Silva, Odete
Fernandes, Miguel
Avelar, Catarina
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  surname: Avelar
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  givenname: Miguel
  surname: Fernandes
  fullname: Fernandes, Miguel
  organization: University of Aveiro
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  fullname: Sá, Juliana
  organization: University of Aveiro
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  givenname: Odete
  orcidid: 0000-0003-3718-9874
  surname: Cruz e Silva
  fullname: Cruz e Silva, Odete
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/35088449$$D View this record in MEDLINE/PubMed
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Tue Apr 29 09:42:35 EDT 2025
Tue Jul 01 02:46:52 EDT 2025
Thu Apr 24 23:01:10 EDT 2025
Wed Jan 22 16:25:56 EST 2025
IsPeerReviewed true
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Issue 9
Keywords ageing
mitophagy
mitochondria
ROS
neurodegeneration
neuron
Huntington
axon
Alzheimer
Parkinson
Language English
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Snippet Mitochondria are associated with various cellular activities critical to homeostasis, particularly in the nervous system. The plastic architecture of the...
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SubjectTerms ageing
Alzheimer
axon
brain
cognitive disorders
energy
homeostasis
Huntington
metabolism
mitochondria
mitophagy
neurodegeneration
neurodegenerative diseases
neuron
neurons
neuropathology
oxidative stress
Parkinson
ROS
stress response
therapeutics
Title Mitochondria, energy, and metabolism in neuronal health and disease
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2F1873-3468.14298
https://www.ncbi.nlm.nih.gov/pubmed/35088449
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