scholarly journals A 1-Month Ketogenic Diet Increased Mitochondrial Mass in Red Gastrocnemius Muscle, but not in the Brain or Liver of Middle-Aged Mice

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2533
Author(s):  
Zeyu Zhou ◽  
Jocelyn Vidales ◽  
José A González-Reyes ◽  
Bradley Shibata ◽  
Keith Baar ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Gastrocnemius Muscle ◽  
Left Lobe ◽  
Middle Aged ◽  
Mitochondrial Content ◽  
Mitochondrial Mass ◽  
Aged Mice ◽  
Fractional Area ◽  
Ketogenic Diets ◽  
The Impact

Alterations in markers of mitochondrial content with ketogenic diets (KD) have been reported in tissues of rodents, but morphological quantification of mitochondrial mass using transmission electron microscopy (TEM), the gold standard for mitochondrial quantification, is needed to further validate these findings and look at specific regions of interest within a tissue. In this study, red gastrocnemius muscle, the prefrontal cortex, the hippocampus, and the liver left lobe were used to investigate the impact of a 1-month KD on mitochondrial content in healthy middle-aged mice. The results showed that in red gastrocnemius muscle, the fractional area of both subsarcolemmal (SSM) and intermyofibrillar (IMM) mitochondria was increased, and this was driven by an increase in the number of mitochondria. Mitochondrial fractional area or number was not altered in the liver, prefrontal cortex, or hippocampus following 1 month of a KD. These results demonstrate tissue-specific changes in mitochondrial mass with a short-term KD and highlight the need to study different muscle groups or tissue regions with TEM to thoroughly determine the effects of a KD on mitochondrial mass.

scholarly journals Vascular mitochondrial respiratory function: the impact of advancing age

2018 ◽  
Vol 315 (6) ◽  
pp. H1660-H1669 ◽  
Author(s):  
Soung Hun Park ◽  
Oh Sung Kwon ◽  
Song-Young Park ◽  
Joshua C. Weavil ◽  
Robert H. I. Andtbacka ◽  
...  
Keyword(s):  
Oxidative Coupling ◽  
Respiratory Function ◽  
Complex I ◽  
Coupling Efficiency ◽  
Middle Aged ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
Age Related ◽  
The Impact ◽  
Mitochondrial Respiratory

Little is known about vascular mitochondrial respiratory function and the impact of age. Therefore, skeletal muscle feed arteries were harvested from young (33 ± 7 yr, n = 10), middle-aged (54 ± 5 yr, n = 10), and old (70 ± 7 yr, n = 10) subjects, and mitochondrial respiration as well as citrate synthase (CS) activity were assessed. Complex I (CI) and complex I + II (CI+II) state 3 respiration were greater in young (CI: 10.4 ± 0.8 pmol·s−1·mg−1 and CI+II: 12.4 ± 0.8 pmol·s−1·mg−1, P < 0.05) than middle-aged (CI: 7 ± 0.6 pmol·s−1·mg−1 and CI+II: 8.3 ± 0.5 pmol·s−1·mg−1) and old (CI: 7.2 ± 0.4 pmol·s−1·mg−1 and CI+II: 7.6 ± 0.5 pmol·s−1·mg−1) subjects and, as in the case of complex II (CII) state 3 respiration, were inversely correlated with age [ r = −0.56 (CI), r = −0.7 (CI+II), and r = 0.4 (CII), P < 0.05]. In contrast, state 4 respiration and mitochondria-specific superoxide levels were not different across groups. The respiratory control ratio was greater in young (2.2 ± 0.2, P < 0.05) than middle-aged and old (1.4 ± 0.1 and 1.1 ± 0.1, respectively) subjects and inversely correlated with age ( r = −0.71, P < 0.05). As CS activity was inversely correlated with age ( r = −0.54, P < 0.05), when normalized for mitochondrial content, the age-related differences and relationships with state 3 respiration were ablated. In contrast, mitochondrion-specific state 4 respiration was now lower in young (15 ± 1.4 pmol·s−1·mg−1·U CS−1, P < 0.05) than middle-aged and old (23.4 ± 3.6 and 27.9 ± 3.4 pmol·s−1·mg−1·U CS−1, respectively) subjects and correlated with age ( r = 0.46, P < 0.05). Similarly, superoxide/CS levels were lower in young (0.07 ± 0.01) than old (0.19 ± 0.41) subjects and correlated with age ( r = 0.44, P < 0.05). Therefore, with aging, vascular mitochondrial respiratory function declines, predominantly as a consequence of falling mitochondrial content. However, per mitochondrion, aging likely results in greater mitochondrion-derived oxidative stress, which may contribute to age-related vascular dysfunction. NEW & NOTEWORTHY This study determined, for the first time, that vascular mitochondrial oxidative respiratory capacity, oxidative coupling efficiency, and mitochondrial content fell progressively with advancing age. In terms of single mitochondrion-specific respiration, the age-related differences were completely ablated and the likelihood of free radical production increased progressively with advancing age. This study reveals that vascular mitochondrial respiratory capacity declines with advancing age, as a consequence of falling mitochondrial content, as does oxidative coupling efficiency.

Fluoxetine Protects against Dendritic Spine Loss in Middle-aged APPswe/PSEN1dE9 Double Transgenic Alzheimer’s Disease Mice

2020 ◽  
Vol 17 (1) ◽  
pp. 93-103 ◽  
Author(s):  
Jing Ma ◽  
Yuan Gao ◽  
Wei Tang ◽  
Wei Huang ◽  
Yong Tang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Early Stage ◽  
Learning Ability ◽  
Middle Aged ◽  
Protein Levels ◽  
Spine Pathology ◽  
The Impact

Background: Studies have suggested that cognitive impairment in Alzheimer’s disease (AD) is associated with dendritic spine loss, especially in the hippocampus. Fluoxetine (FLX) has been shown to improve cognition in the early stage of AD and to be associated with diminishing synapse degeneration in the hippocampus. However, little is known about whether FLX affects the pathogenesis of AD in the middle-tolate stage and whether its effects are correlated with the amelioration of hippocampal dendritic dysfunction. Previously, it has been observed that FLX improves the spatial learning ability of middleaged APP/PS1 mice. Objective: In the present study, we further characterized the impact of FLX on dendritic spines in the hippocampus of middle-aged APP/PS1 mice. Results: It has been found that the numbers of dendritic spines in dentate gyrus (DG), CA1 and CA2/3 of hippocampus were significantly increased by FLX. Meanwhile, FLX effectively attenuated hyperphosphorylation of tau at Ser396 and elevated protein levels of postsynaptic density 95 (PSD-95) and synapsin-1 (SYN-1) in the hippocampus. Conclusion: These results indicated that the enhanced learning ability observed in FLX-treated middle-aged APP/PS1 mice might be associated with remarkable mitigation of hippocampal dendritic spine pathology by FLX and suggested that FLX might be explored as a new strategy for therapy of AD in the middle-to-late stage.

scholarly journals The Impact of Work Hours on Depressive Symptoms among Koreans Aged 45 and Over

2021 ◽  
Vol 18 (3) ◽  
pp. 853
Author(s):  
Juyeong Kim ◽  
Eun-Cheol Park
Keyword(s):  
Older Adults ◽  
Depressive Symptoms ◽  
Social Services ◽  
Depression Scale ◽  
Epidemiological Studies ◽  
Work Hours ◽  
Middle Aged ◽  
Health Studies ◽  
Males And Females ◽  
The Impact

Background: Given the documented importance of employment for middle-aged and older adults’ mental health, studies of the association between their number of work hours and depressive symptoms are needed. Objectives: To examine the association between the number of work hours and depressive symptoms in Korean aged 45 and over. Methods: We used data from the first wave to fourth wave of the Korea Longitudinal Study of Aging. Using the first wave at baseline, data included 9845 individuals. Depressive symptoms were measured using the 10-item Center for Epidemiological Studies Depression scale. We performed a longitudinal analysis to estimate the prevalence of depressive symptoms by work hours. Results: Both unemployed males and females aged 45–65 years were associated with higher depressive symptoms (β = 0.59, p < 0.001; β = 0.32, p < 0.001). Females working ≥ 69 h were associated with higher depressive symptoms compared to those working 41–68 h (β = 0.25, p = 0.013). Among those both middle-aged and older adults, both males and females unemployed were associated with higher depressive symptoms. Those middle-aged female working ≥69 h were associated with higher depressive symptoms. Conclusions: An increase in depressive symptoms was associated with unemployed males and females working ≥69 h compared to those working 41–68 h. Although this association was found among middle-aged individuals, a decrease in depressive symptoms in both sexes was associated with working 1–40 h. Depressive symptoms should decrease by implementing employment policies and social services to encourage employers to support middle-aged and older adults in the workforce considering their sex and age differences.

TNF signaling via TNF receptors does not mediate the effects of short-term exercise on cognition, anxiety and depressive-like behaviors in middle-aged mice

2021 ◽  
pp. 113269
Author(s):  
Gaurav Singhal ◽  
Magdalene C. Jawahar ◽  
Julie Morgan ◽  
Frances Corrigan ◽  
Emily J. Jaehne ◽  
...  
Keyword(s):  
Tnf Receptors ◽  
Middle Aged ◽  
Short Term ◽  
Aged Mice

scholarly journals Developmental up-regulation of NMDA receptors in the prefrontal cortex and hippocampus of mGlu5 receptor knock-out mice

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Tiziana Imbriglio ◽  
Remy Verhaeghe ◽  
Nico Antenucci ◽  
Stefania Maccari ◽  
Giuseppe Battaglia ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nmda Receptor ◽  
Metabotropic Glutamate Receptors ◽  
Adult Life ◽  
Developmental Time ◽  
Postnatal Life ◽  
Developmental Studies ◽  
Knock Out ◽  
Nmda Receptor Subunits ◽  
The Impact

AbstractmGlu5 metabotropic glutamate receptors are highly expressed and functional in the early postnatal life, and are known to positively modulate NMDA receptor function. Here, we examined the expression of NMDA receptor subunits and interneuron-related genes in the prefrontal cortex and hippocampus of mGlu5−/− mice and wild-type littermates at three developmental time points (PND9, − 21, and − 75). We were surprised to find that expression of all NMDA receptor subunits was greatly enhanced in mGlu5−/− mice at PND21. In contrast, at PND9, expression of the GluN2B subunit was enhanced, whereas expression of GluN2A and GluN2D subunits was reduced in both regions. These modifications were transient and disappeared in the adult life (PND75). Changes in the transcripts of interneuron-related genes (encoding parvalbumin, somatostatin, vasoactive intestinal peptide, reelin, and the two isoforms of glutamate decarboxylase) were also observed in mGlu5−/− mice across postnatal development. For example, the transcript encoding parvalbumin was up-regulated in the prefrontal cortex of mGlu5−/− mice at PND9 and PND21, whereas it was significantly reduced at PND75. These findings suggest that in mGlu5−/− mice a transient overexpression of NMDA receptor subunits may compensate for the lack of the NMDA receptor partner, mGlu5. Interestingly, in mGlu5−/− mice the behavioral response to the NMDA channel blocker, MK-801, was significantly increased at PND21, and largely reduced at PND75. The impact of adaptive changes in the expression of NMDA receptor subunits should be taken into account when mGlu5−/− mice are used for developmental studies.

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