The role of mitochondrial ROS in the aging brain
The brain is the most complex human organ, consuming more energy than any other tissue in proportion to its size. It relies heavily on mitochondria to produce energy and is made up of mitotic and postmitotic cells that need to closely coordinate their metabolism to maintain essential bodily function...
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| Published in | FEBS letters Vol. 592; no. 5; pp. 743 - 758 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
England
01.03.2018
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | The brain is the most complex human organ, consuming more energy than any other tissue in proportion to its size. It relies heavily on mitochondria to produce energy and is made up of mitotic and postmitotic cells that need to closely coordinate their metabolism to maintain essential bodily functions. During aging, damaged mitochondria that produce less ATP and more reactive oxygen species (ROS) accumulate. The current consensus is that ROS cause oxidative stress, damaging mitochondria and resulting in an energetic crisis that triggers neurodegenerative diseases and accelerates aging. However, in model organisms, increasing mitochondrial ROS (mtROS) in the brain extends lifespan, suggesting that ROS may participate in signaling that protects the brain. Here, we summarize the mechanisms by which mtROS are produced at the molecular level, how different brain cells and regions produce different amounts of mtROS, and how mtROS levels change during aging. Finally, we critically discuss the possible roles of ROS in aging as signaling molecules and damaging agents, addressing whether age‐associated increases in mtROS are a cause or a consequence of aging. |
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| AbstractList | The brain is the most complex human organ, consuming more energy than any other tissue in proportion to its size. It relies heavily on mitochondria to produce energy and is made up of mitotic and postmitotic cells that need to closely coordinate their metabolism to maintain essential bodily functions. During aging, damaged mitochondria that produce less
ATP
and more reactive oxygen species (
ROS
) accumulate. The current consensus is that
ROS
cause oxidative stress, damaging mitochondria and resulting in an energetic crisis that triggers neurodegenerative diseases and accelerates aging. However, in model organisms, increasing mitochondrial
ROS
(mt
ROS
) in the brain extends lifespan, suggesting that
ROS
may participate in signaling that protects the brain. Here, we summarize the mechanisms by which mt
ROS
are produced at the molecular level, how different brain cells and regions produce different amounts of mt
ROS
, and how mt
ROS
levels change during aging. Finally, we critically discuss the possible roles of
ROS
in aging as signaling molecules and damaging agents, addressing whether age‐associated increases in mt
ROS
are a cause or a consequence of aging. The brain is the most complex human organ, consuming more energy than any other tissue in proportion to its size. It relies heavily on mitochondria to produce energy and is made up of mitotic and postmitotic cells that need to closely coordinate their metabolism to maintain essential bodily functions. During aging, damaged mitochondria that produce less ATP and more reactive oxygen species (ROS) accumulate. The current consensus is that ROS cause oxidative stress, damaging mitochondria and resulting in an energetic crisis that triggers neurodegenerative diseases and accelerates aging. However, in model organisms, increasing mitochondrial ROS (mtROS) in the brain extends lifespan, suggesting that ROS may participate in signaling that protects the brain. Here, we summarize the mechanisms by which mtROS are produced at the molecular level, how different brain cells and regions produce different amounts of mtROS, and how mtROS levels change during aging. Finally, we critically discuss the possible roles of ROS in aging as signaling molecules and damaging agents, addressing whether age-associated increases in mtROS are a cause or a consequence of aging. The brain is the most complex human organ, consuming more energy than any other tissue in proportion to its size. It relies heavily on mitochondria to produce energy and is made up of mitotic and postmitotic cells that need to closely coordinate their metabolism to maintain essential bodily functions. During aging, damaged mitochondria that produce less ATP and more reactive oxygen species (ROS) accumulate. The current consensus is that ROS cause oxidative stress, damaging mitochondria and resulting in an energetic crisis that triggers neurodegenerative diseases and accelerates aging. However, in model organisms, increasing mitochondrial ROS (mtROS) in the brain extends lifespan, suggesting that ROS may participate in signaling that protects the brain. Here, we summarize the mechanisms by which mtROS are produced at the molecular level, how different brain cells and regions produce different amounts of mtROS, and how mtROS levels change during aging. Finally, we critically discuss the possible roles of ROS in aging as signaling molecules and damaging agents, addressing whether age-associated increases in mtROS are a cause or a consequence of aging.The brain is the most complex human organ, consuming more energy than any other tissue in proportion to its size. It relies heavily on mitochondria to produce energy and is made up of mitotic and postmitotic cells that need to closely coordinate their metabolism to maintain essential bodily functions. During aging, damaged mitochondria that produce less ATP and more reactive oxygen species (ROS) accumulate. The current consensus is that ROS cause oxidative stress, damaging mitochondria and resulting in an energetic crisis that triggers neurodegenerative diseases and accelerates aging. However, in model organisms, increasing mitochondrial ROS (mtROS) in the brain extends lifespan, suggesting that ROS may participate in signaling that protects the brain. Here, we summarize the mechanisms by which mtROS are produced at the molecular level, how different brain cells and regions produce different amounts of mtROS, and how mtROS levels change during aging. Finally, we critically discuss the possible roles of ROS in aging as signaling molecules and damaging agents, addressing whether age-associated increases in mtROS are a cause or a consequence of aging. |
| Author | Sanz, Alberto Stefanatos, Rhoda |
| Author_xml | – sequence: 1 givenname: Rhoda surname: Stefanatos fullname: Stefanatos, Rhoda organization: Newcastle University – sequence: 2 givenname: Alberto surname: Sanz fullname: Sanz, Alberto email: alberto.sanz@newcastle.ac.uk organization: Newcastle University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29106705$$D View this record in MEDLINE/PubMed |
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| Keywords | aging brain mitochondria signalling reactive oxygen species |
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| SubjectTerms | Adenosine Triphosphate - genetics Adenosine Triphosphate - metabolism aging Aging - genetics Aging - metabolism Aging - pathology Animals brain Brain - metabolism Brain - pathology energy Energy Metabolism Humans longevity metabolism mitochondria Mitochondria - genetics Mitochondria - metabolism Mitochondria - pathology mitosis Neurodegenerative Diseases - genetics Neurodegenerative Diseases - metabolism Neurodegenerative Diseases - pathology oxidative stress reactive oxygen species Reactive Oxygen Species - metabolism Signal Transduction signalling |
| Title | The role of mitochondrial ROS in the aging brain |
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