Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice
Joint Authors
Grewal, Rekha
Eckert, Gunter P.
Reutzel, Martina
Dilberger, Benjamin
Silaidos, Carmina
Joppe, Aljoscha
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-04-15
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Brain aging is one of the major risk factors for the development of several neurodegenerative diseases.
Therefore, mitochondrial dysfunction plays an important role in processes of both, brain aging and neurodegeneration.
Aged mice including NMRI mice are established model organisms to study physiological and molecular mechanisms of brain aging.
However, longitudinal data evaluated in one cohort are rare but are important to understand the aging process of the brain throughout life, especially since pathological changes early in life might pave the way to neurodegeneration in advanced age.
To assess the longitudinal course of brain aging, we used a cohort of female NMRI mice and measured brain mitochondrial function, cognitive performance, and molecular markers every 6 months until mice reached the age of 24 months.
Furthermore, we measured citrate synthase activity and respiration of isolated brain mitochondria.
Mice at the age of three months served as young controls.
At six months of age, mitochondria-related genes (complex IV, creb-1, β-AMPK, and Tfam) were significantly elevated.
Brain ATP levels were significantly reduced at an age of 18 months while mitochondria respiration was already reduced in middle-aged mice which is in accordance with the monitored impairments in cognitive tests.
mRNA expression of genes involved in mitochondrial biogenesis (cAMP response element-binding protein 1 (creb-1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α), nuclear respiratory factor-1 (Nrf-1), mitochondrial transcription factor A (Tfam), growth-associated protein 43 (GAP43), and synaptophysin 1 (SYP1)) and the antioxidative defense system (catalase (Cat) and superoxide dismutase 2 (SOD2)) was measured and showed significantly decreased expression patterns in the brain starting at an age of 18 months.
BDNF expression reached, a maximum after 6 months.
On the basis of longitudinal data, our results demonstrate a close connection between the age-related decline of cognitive performance, energy metabolism, and mitochondrial biogenesis during the physiological brain aging process.
American Psychological Association (APA)
Reutzel, Martina& Grewal, Rekha& Dilberger, Benjamin& Silaidos, Carmina& Joppe, Aljoscha& Eckert, Gunter P.. 2020. Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1204446
Modern Language Association (MLA)
Reutzel, Martina…[et al.]. Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1204446
American Medical Association (AMA)
Reutzel, Martina& Grewal, Rekha& Dilberger, Benjamin& Silaidos, Carmina& Joppe, Aljoscha& Eckert, Gunter P.. Cerebral Mitochondrial Function and Cognitive Performance during Aging: A Longitudinal Study in NMRI Mice. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1204446
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204446