scholarly journals Effect of aging on the chaperone-like function of human α-crystallin assessed by three methods

1997 ◽  
Vol 328 (3) ◽  
pp. 763-768 ◽  
Author(s):  
K. Barry DERHAM ◽  
J. John HARDING

α-Crystallin can function as a molecular chaperone by preventing unwanted interactions. This paper presents the effects of aging and cataract on the chaperone-like properties of α-crystallin from soluble fractions from the cortex and nucleus of human lenses by using three assays: enzyme inactivation and two turbidity experiments. The three methods complemented each other. There was no decrease with age of chaperone-like function of cortical α-low and α-high crystallin. Nuclear α-low crystallin showed a decrease, whereas α-high crystallin showed no age-related change but its protective effect was diminished. Results from the nucleus of 40-year-old cataractous lenses seemed similar to those for clear lenses of equivalent age, whereas 80-year-old cataractous lenses showed decreased chaperone-like behaviour.

Amino Acids ◽  
2021 ◽  
Author(s):  
Tomohisa Yoshimura ◽  
Yuki Inokuchi ◽  
Chikako Mutou ◽  
Takanobu Sakurai ◽  
Tohru Nagahama ◽  
...  

AbstractTaurine, a sulfur-containing amino acid, occurs at high concentrations in the skin, and plays a role in maintaining the homeostasis of the skin. We investigated the effects of aging on the content and localization of taurine in the skin of mice and rats. Taurine was extracted from the skin samples of hairless mice and Sprague Dawley rats, and the taurine content of the skin was determined by high-performance liquid chromatography (HPLC). The results of the investigation revealed that the taurine content in both the dermis and epidermis of hairless mice declined significantly with age. Similar age-related decline in the skin taurine content was also observed in rats. In contrast, the taurine content in the sole remained unchanged with age. An immunohistochemical analysis also revealed a decreased skin taurine content in aged animals compared with younger animals, although no significant differences in the localization of taurine were observed between the two age groups. Supplementation of the drinking water of aged mice with 3% (w/v) taurine for 4 weeks increased the taurine content of the epidermis, but not the dermis. The present study showed for the first time that the taurine content of the skin decreased with age in mice and rats, which may be related to the impairment of the skin homeostasis observed with aging. The decreased taurine content of the epidermis in aged animals was able to be rescued by taurine supplementation.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Diana S. Cortes ◽  
Christina Tornberg ◽  
Tanja Bänziger ◽  
Hillary Anger Elfenbein ◽  
Håkan Fischer ◽  
...  

AbstractAge-related differences in emotion recognition have predominantly been investigated using static pictures of facial expressions, and positive emotions beyond happiness have rarely been included. The current study instead used dynamic facial and vocal stimuli, and included a wider than usual range of positive emotions. In Task 1, younger and older adults were tested for their abilities to recognize 12 emotions from brief video recordings presented in visual, auditory, and multimodal blocks. Task 2 assessed recognition of 18 emotions conveyed by non-linguistic vocalizations (e.g., laughter, sobs, and sighs). Results from both tasks showed that younger adults had significantly higher overall recognition rates than older adults. In Task 1, significant group differences (younger > older) were only observed for the auditory block (across all emotions), and for expressions of anger, irritation, and relief (across all presentation blocks). In Task 2, significant group differences were observed for 6 out of 9 positive, and 8 out of 9 negative emotions. Overall, results indicate that recognition of both positive and negative emotions show age-related differences. This suggests that the age-related positivity effect in emotion recognition may become less evident when dynamic emotional stimuli are used and happiness is not the only positive emotion under study.


2002 ◽  
Vol 13 (12) ◽  
pp. 4243-4255 ◽  
Author(s):  
Julie E. Legakis ◽  
Jay I. Koepke ◽  
Chris Jedeszko ◽  
Ferdous Barlaskar ◽  
Laura J. Terlecky ◽  
...  

The molecular mechanisms of peroxisome biogenesis have begun to emerge; in contrast, relatively little is known about how the organelle functions as cells age. In this report, we characterize age-related changes in peroxisomes of human cells. We show that aging compromises peroxisomal targeting signal 1 (PTS1) protein import, affecting in particular the critical antioxidant enzyme catalase. The number and appearance of peroxisomes are altered in these cells, and the organelles accumulate the PTS1-import receptor, Pex5p, on their membranes. Concomitantly, cells produce increasing amounts of the toxic metabolite hydrogen peroxide, and we present evidence that this increased load of reactive oxygen species may further reduce peroxisomal protein import and exacerbate the effects of aging.


2008 ◽  
Vol 294 (4) ◽  
pp. H1562-H1570 ◽  
Author(s):  
Hélène Bulckaen ◽  
Gaétan Prévost ◽  
Eric Boulanger ◽  
Géraldine Robitaille ◽  
Valérie Roquet ◽  
...  

The age-related impairment of endothelium-dependent vasodilatation contributes to increased cardiovascular risk in the elderly. For primary and secondary prevention, aspirin can reduce the incidence of cardiovascular events in this patient population. The present work evaluated the effect of low-dose aspirin on age-related endothelial dysfunction in C57B/J6 aging mice and investigated its protective antioxidative effect. Age-related endothelial dysfunction was assessed by the response to acetylcholine of phenylephrine-induced precontracted aortic segments isolated from 12-, 36-, 60-, and 84-wk-old mice. The effect of low-dose aspirin was examined in mice presenting a decrease in endothelial-dependent relaxation (EDR). The effects of age and aspirin treatment on structural changes were determined in mouse aortic sections. The effect of aspirin on the oxidative stress markers malondialdehyde and 8-hydroxy-2′-deoxyguanosine (8-OhdG) was also quantified. Compared with that of 12-wk-old mice, the EDR was significantly reduced in 60- and 84-wk-old mice ( P < 0.05); 68-wk-old mice treated with aspirin displayed a higher EDR compared with control mice of the same age (83.9 ± 4 vs. 66.3 ± 5%; P < 0.05). Aspirin treatment decreased 8-OHdG levels ( P < 0.05), but no significant effect on intima/media thickness ratio was observed. The protective effect of aspirin was not observed when treatment was initiated in older mice (96 wk of age). It was found that low-dose aspirin is able to prevent age-related endothelial dysfunction in aging mice. However, the absence of this effect in the older age groups demonstrates that treatment should be initiated early on. The underlying mechanism may involve the protective effect of aspirin against oxidative stress.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 856
Author(s):  
Eun Young Kim ◽  
Stuart E. Dryer

Canonical transient receptor potential 6 (TRPC6) channels have been implicated in familial and acquired forms of focal and segmental glomerulosclerosis (FSGS) in patients and animal models, as well as in renal fibrosis following ureteral obstruction in mice. Aging also evokes declines in renal function owing to effects on almost every renal compartment in humans and rodents. Here, we have examined the role of TRPC6 in driving inflammation and fibrosis during aging in Sprague-Dawley rats. This was assessed in rats with non-functional TRPC6 channels owing to CRISPR-Cas9 deletion of a portion of the ankyrin repeat domain required for the assembly of functional TRPC6 channels (Trpc6del/del rats). Wild-type littermates (Trpc6wt/wt rats) were used as controls. Animals were evaluated at 2 months and 12 months of age. There was no sign of kidney disease at 2 months of age, regardless of genotype. However, by 12 months of age, all rats examined showed declines in renal function associated with albuminuria, azotemia and increased urine excretion of β2–microglobulin, a marker for proximal tubule pathology. These changes were equally severe in Trpc6wt/wt and Trpc6del/del rats. We also observed age-related increases in renal cortical expression of markers of fibrosis (α-smooth muscle actin and vimentin) and inflammation (NLRP3 and pro-IL−1β), and there was no detectable protective effect of TRPC6 inactivation. Tubulointerstitial fibrosis assessed from histology also appeared equally severe in Trpc6wt/wt and Trpc6del/del rats. By contrast, glomerular pathology, blindly scored from histological sections, suggested a significant protective effect of TRPC6 inactivation, but only within the glomerular compartment.


1997 ◽  
Vol 74 (3) ◽  
pp. 152-159 ◽  
Author(s):  
KAREN HOLOPIGIAN ◽  
WILLIAM SEIPLE ◽  
VIVIENNE GREENSTEIN ◽  
DANIEL KIM ◽  
RONALD E. CARR

1992 ◽  
Vol 263 (5) ◽  
pp. R1099-R1103 ◽  
Author(s):  
P. C. Zee ◽  
R. S. Rosenberg ◽  
F. W. Turek

The phase angle of entrainment of the circadian rhythm of the locomotor activity rhythm to a light-dark (LD) cycle was examined in young (2-5 mo old) and middle-aged (13-16 mo old) hamsters. An age-related phase advance in the onset of locomotor activity relative to lights off was seen during stable entrainment to a 14:10-h LD cycle. In addition, the effects of age on the rate of reentrainment of the circadian rhythm of locomotor activity were examined by subjecting young and middle-aged hamsters to either an 8-h advance or delay shift of the LD cycle. Middle-aged hamsters resynchronized more rapidly after a phase advance of the LD cycle than did young hamsters, whereas young hamsters were able to phase delay more rapidly than middle-aged hamsters. The age-related phase advance of activity onset under entrained conditions, and the alteration of responses in middle-aged hamsters reentraining to a phase-shifted LD cycle, may be due to the shortening of the free-running period of the circadian rhythm of locomotor activity with advancing age that has previously been observed in this species.


2018 ◽  
Vol 120 (6) ◽  
pp. 2939-2952 ◽  
Author(s):  
Samira Anderson ◽  
Robert Ellis ◽  
Julie Mehta ◽  
Matthew J. Goupell

The effects of aging and stimulus configuration on binaural masking level differences (BMLDs) were measured behaviorally and electrophysiologically, using the frequency-following response (FFR) to target brainstem/midbrain encoding. The tests were performed in 15 younger normal-hearing (<30 yr) and 15 older normal-hearing (>60 yr) participants. The stimuli consisted of a 500-Hz target tone embedded in a narrowband (50-Hz bandwidth) or wideband (1,500-Hz bandwidth) noise masker. The interaural phase conditions included NoSo (tone and noise presented interaurally in-phase), NoSπ (noise presented interaurally in-phase and tone presented out-of-phase), and NπSo (noise presented interaurally out-of-phase and tone presented in-phase) configurations. In the behavioral experiment, aging reduced the magnitude of the BMLD. The magnitude of the BMLD was smaller for the NoSo–NπSo threshold difference compared with the NoSo–NoSπ threshold difference, and it was also smaller in narrowband compared with wideband conditions, consistent with previous measurements. In the electrophysiology experiment, older participants had reduced FFR magnitudes and smaller differences between configurations. There were significant changes in FFR magnitude between the NoSo to NoSπ configurations but not between the NoSo to NπSo configurations. The age-related reduction in FFR magnitudes suggests a temporal processing deficit, but no correlation was found between FFR magnitudes and behavioral BMLDs. Therefore, independent mechanisms may be contributing to the behavioral and neural deficits. Specifically, older participants had higher behavioral thresholds than younger participants for the NoSπ and NπSo configurations but had equivalent thresholds for the NoSo configuration. However, FFR magnitudes were reduced in older participants across all configurations. NEW & NOTEWORTHY Behavioral and electrophysiological testing reveal an aging effect for stimuli presented in wideband and narrowband noise conditions, such that behavioral binaural masking level differences and subcortical spectral magnitudes are reduced in older compared with younger participants. These deficits in binaural processing may limit the older participant's ability to use spatial cues to understand speech in environments containing competing sound sources.


Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2531
Author(s):  
Amandine Grimm

The brain is the most energy-consuming organ of the body and impairments in brain energy metabolism will affect neuronal functionality and viability. Brain aging is marked by defects in energetic metabolism. Abnormal tau protein is a hallmark of tauopathies, including Alzheimer’s disease (AD). Pathological tau was shown to induce bioenergetic impairments by affecting mitochondrial function. Although it is now clear that mutations in the tau-coding gene lead to tau pathology, the causes of abnormal tau phosphorylation and aggregation in non-familial tauopathies, such as sporadic AD, remain elusive. Strikingly, both tau pathology and brain hypometabolism correlate with cognitive impairments in AD. The aim of this review is to discuss the link between age-related decrease in brain metabolism and tau pathology. In particular, the following points will be discussed: (i) the common bioenergetic features observed during brain aging and tauopathies; (ii) how age-related bioenergetic defects affect tau pathology; (iii) the influence of lifestyle factors known to modulate brain bioenergetics on tau pathology. The findings compiled here suggest that age-related bioenergetic defects may trigger abnormal tau phosphorylation/aggregation and cognitive impairments after passing a pathological threshold. Understanding the effects of aging on brain metabolism may therefore help to identify disease-modifying strategies against tau-induced neurodegeneration.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A164-A166
Author(s):  
E Taylor ◽  
W D Killgore

Abstract Introduction Mild cognitive impairment (MCI), Alzheimer’s disease (AD), and dementia are common forms of neurodegenerative cognitive decline in aging populations. Alertness, attention, and sleep patterns are often impaired in dementia and MCI and can affect ongoing cognition. Given the current lack of treatment options, it is important to identify protective factors. Caffeine is a commonly consumed substance which has been demonstrated in previous observational studies to have a protective effect on the onset of MCI and the progression of MCI to AD. Methods A meta-analysis of longitudinal prospective cohort studies published up to December 2017 was conducted comparing highest vs lowest reported category of caffeine consumption on neurodegenerative outcomes. Three databases were searched including PubMed, EMBASE, and Web of Science. Two investigators independently extracted data and assessed study quality. 13 studies were selected including 94880 participants. The effect size was reported as RRs with ORs and HRs treated as approximations of the RRs. Results A meta-analysis conducted using random effects showed a pooled RR of .84, 95% CI (0.75, 0.93) indicating a moderate protective effect in higher levels of caffeine consumption compared to lower levels. By outcome, AD had a RR of 1.14 with 95% CI (0.69, 1.90); dementia had a RR of 0.81 (0.72, 0.92); cognitive decline had a RR of 0.81 (0.55, 1.18); and MCI had a RR of 0.78 (0.65, 0.93). Conclusion Overall this meta-analysis suggests that compared with the lowest category, the highest caffeine intake category is inversely related to the incidence of age-related cognitive disorders, with this relationship being most apparent for dementia and MCI. Given that caffeine is well accepted and consumed widely in a variety of forms, caffeine in moderate doses, may prove beneficial in sustaining cognitive functioning. Further work will examine the hypothesis that increased alertness and attention with caffeine may sustain cognition through use dependent plasticity or circadian modulation. Support None


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