Age
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Coenzyme Q10 (CoQ) is widely available as a dietary supplement and remains under consideration as a treatment for age-associated neurodegenerative conditions. However, no studies have determined if supplementation, initiated relatively late in life, could have beneficial effects on mild functional impairments associated with normal brain aging. Accordingly, the current study assessed the effect of CoQ intake in older mice for which cognitive and psychomotor impairments were already evident. ⋯ Protein oxidative damage was decreased in the mitochondria from the heart, liver, and skeletal muscle of the high-CoQ-supplemented mice and, to some extent, in the brain mitochondria. Contrasting with the deleterious effect of long-term CoQ supplementation initiated during young adulthood previously published, this study suggests that CoQ improves spatial learning and attenuates oxidative damage when administered in relatively high doses and delayed until early senescence, after age-related declines have occurred. Thus, in individuals with age-associated symptoms of cognitive decline, high-CoQ intake may be beneficial.
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Mild traumatic brain injury (mTBI) represents a major and increasing public health concern and is both the most frequent cause of mortality and disability in young adults and a chief cause of morbidity in the elderly. Albeit mTBI patients do not show clear structural brain defects and, generally, do not require hospitalization, they frequently suffer from long-lasting cognitive, behavioral, and emotional problems. No effective pharmaceutical therapy is available, and existing treatment chiefly involves intensive care management after injury. ⋯ Ex-4 proved well-tolerated and fully ameliorated mTBI-induced deficits in novel object recognition 7 and 30 days post-trauma. Less mTBI-induced impairment was evident in Y-maze, elevated plus maze, and passive avoidance paradigms, but when impairment was apparent Ex-4 induced amelioration. Together, these results suggest that Ex-4 may act as a neurotrophic/neuroprotective drug to minimize mTBI impairment.
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Conventionally, sarcopenia is defined by muscle mass and physical performance. We hypothesized that the disability caused by sarcopenia and sarcopenic obesity was related to the amount of adiposity or body weight bearing on a unit of muscle mass, or the adiposity to muscle ratio. We therefore examined whether this ratio could predict physical limitation by secondary analysis of the data in our previous study. ⋯ In men, the adiposity to muscle ratios, namely total body fat to lower-limb muscle mass, total body fat to fat-free mass (FFM), and body weight to FFM, were predictive of physical limitation before and after adjustment for the covariates: age, Mini-mental Status Examination score, Geriatric Depression Scale score >8, and the diagnosis of chronic obstructive pulmonary disease, diabetes mellitus, hypertension, heart disease, and stroke (all p values < 0.001), when the total body fat to lower-limb muscle mass ratio was greater than or equal to 0.75. In women, throughout the entire range of that ratio, all three adiposity to muscle ratios were associated with physical limitation 4 years later both before and after adjustment for the same set of covariates (all p values < 0.05). Sarcopenia and sarcopenic obesity as measured by the body weight or adiposity bearing on a unit of muscle mass (the adiposity to muscle ratio) could predict incident or worsening physical limitation in older women across the entire range of the total body fat to lower-limb muscle mass ratio; and in older men when this ratio was equal to or greater than 0.75.
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In this study, we investigated 102 single-nucleotide polymorphisms (SNPs) covering the common genetic variation in 16 genes recurrently regarded as candidates for human longevity: APOE; ACE; CETP; HFE; IL6; IL6R; MTHFR; TGFB1; APOA4; APOC3; SIRTs 1, 3, 6; and HSPAs 1A, 1L, 14. In a case-control study of 1,089 oldest-old (ages 92-93) and 736 middle-aged Danes, the minor allele frequency (MAF) of rs769449 (APOE) was significantly decreased in the oldest-old, while the MAF of rs9923854 (CETP) was significantly enriched. These effects were supported when investigating 1,613 oldest-old (ages 95-110) and 1,104 middle-aged Germans. rs769449 was in modest linkage equilibrium (R (2)=0.55) with rs429358 of the APOE-ε4 haplotype and adjusting for rs429358 eliminated the association of rs769449, indicating that the association likely reflects the well-known effect of rs429358. ⋯ Since rs2069827 was located in a putative transcription factor binding site, quantitative RNA expression studies were conducted. However, no difference in IL6 expression was observed between rs2069827 genotype groups. In conclusion, we here support and expand the evidence suggesting that genetic variation in APOE, CETP, and IL6, and possible HSPA14, is associated with human longevity.
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Older adults require more time to reweight sensory information for maintaining balance that could potentially lead to increased incidence of falling in rapidly changing or cognitively demanding environments. In this study, we manipulated the visual surround information during a collision avoidance task in order to investigate how young and elderly adults engage in sensory reweighting under conditions of visual anticipation. Sixteen healthy elderly (age: 71.5 ± 4.9 years; height: 159.3 ± 6.6 cm; mass: 73.3 ± 3.3 kg) and 20 young (age: 22.8 ± 3.3 years; height: 174.4 ± 10.7 cm; mass: 70.1 ± 13.9 kg) participants stood for 240 s on a force platform under two experimental conditions: quiet standing and standing while anticipating randomly approaching virtual objects to be avoided. ⋯ In addition, both young and elderly participants were similarly affected by the degradation or removal of the visual surround. These findings suggest that sensory reweighting in a dynamic virtual environment that evokes visual anticipation interacts with postural state anxiety regardless of age. Elderly show less efficient sensory reweighting in quiet standing due to greater visual field dependence possibly associated with fear of falling.