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Maintaining and increasing walking speed in old age is clinically important because this activity of daily living predicts functional and clinical state. We reviewed evidence for the biomechanical mechanisms of how strength and power training increase gait speed in old adults. A systematic search yielded only four studies that reported changes in selected gait biomechanical variables after an intervention. A secondary analysis of 20 studies revealed an association of r(2) = 0.21 between the 22% and 12% increase, respectively, in quadriceps strength and gait velocity in 815 individuals age 72. In 6 studies, there was a correlation of r(2) = 0.16 between the 19% and 9% gains in plantarflexion strength and gait speed in 240 old volunteers age 75. In 8 studies, there was zero association between the 35% and 13% gains in leg mechanical power and gait speed in 150 old adults age 73. To increase the efficacy of intervention studies designed to improve gait speed and other critical mobility functions in old adults, there is a need for a paradigm shift from conventional (clinical) outcome assessments to more sophisticated biomechanical analyses that examine joint kinematics, kinetics, energetics, muscle-tendon function, and musculoskeletal modeling before and after interventions.
Age-related changes in prefrontal activity during walking in dual-task situations: A fNIRS study
(2014)
Background: Previous studies suggest that the human gait is under control of higher-order cognitive processes, located in the frontal lobes, such that an age-related degradation of cognitive capabilities has a negative impact on gait.
Results: Our behavioral data partly confirm previous accounts on higher dual-task costs in stepping parameters (i.e., decreased step duration) in old age, particularly with a visual task and negative dual-task cost (i.e., improved performance) during the verbal task in young adults. Functional imaging data revealed little change of prefrontal activation from single- to dual-task walking in young individuals. In the elderly, however, prefrontal activation substantially decreased during dual-task walking with a complex visual task.
Conclusion: We interpret these findings as evidence for a shift of processing resources from the prefrontal cortex to other brain regions when seniors face the challenge of walking and concurrently executing a visually demanding task. (C) 2014 Elsevier B.V. All rights reserved.
Scanpaths have played an important role in classic research on reading behavior. Nevertheless, they have largely been neglected in later research perhaps due to a lack of suitable analytical tools. Recently, von der Malsburg and Vasishth (2011) proposed a new measure for quantifying differences between scanpaths and demonstrated that this measure can recover effects that were missed with the traditional eyetracking measures. However, the sentences used in that study were difficult to process and scanpath effects accordingly strong. The purpose of the present study was to test the validity, sensitivity, and scope of applicability of the scanpath measure, using simple sentences that are typically read from left to right. We derived predictions for the regularity of scanpaths from the literature on oculomotor control, sentence processing, and cognitive aging and tested these predictions using the scanpath measure and a large database of eye movements. All predictions were confirmed: Sentences with short words and syntactically more difficult sentences elicited more irregular scanpaths. Also, older readers produced more irregular scanpaths than younger readers. In addition, we found an effect that was not reported earlier: Syntax had a smaller influence on the eye movements of older readers than on those of young readers. We discuss this interaction of syntactic parsing cost with age in terms of shifts in processing strategies and a decline of executive control as readers age. Overall, our results demonstrate the validity and sensitivity of the scanpath measure and thus establish it as a productive and versatile tool for reading research.
As indicated by previous research, aging is associated with a decline in working memory (WM) functioning, related to alterations in fronto-parietal neural activations. At the same time, previous studies showed that WM training in older adults may improve the performance in the trained task (training effect), and more importantly, also in untrained WM tasks (transfer effects). However, neural correlates of these transfer effects that would improve understanding of its underlying mechanisms, have not been shown in older participants as yet. In this study, we investigated blood-oxygen-level-dependent (BOLD) signal changes during n-back performance and an untrained delayed recognition (Sternberg) task following 12 sessions (45 min each) of adaptive n-back training in older adults. The Sternberg task used in this study allowed to test for neural training effects independent of specific task affordances of the trained task and to separate maintenance from updating processes. Thirty-two healthy older participants (60-75 years) were assigned either to an n-back training or a no-contact control group. Before (t1) and after (t2) training/waiting period, both the n-back task and the Sternberg task were conducted while BOLD signal was measured using functional Magnetic Resonance Imaging (fMRI) in all participants. In addition, neuropsychological tests were performed outside the scanner. WM performance improved with training and behavioral transfer to tests measuring executive functions, processing speed, and fluid intelligence was found. In the training group, BOLD signal in the right lateral middle frontal gyrus/caudal superior frontal sulcus (Brodmann area, BA 6/8) decreased in both the trained n-back and the updating condition of the untrained Sternberg task at t2, compared to the control group. fMRI findings indicate a training-related increase in processing efficiency of WM networks, potentially related to the process of WM updating. Performance gains in untrained tasks suggest that transfer to other cognitive tasks remains possible in aging. (C) 2016 Elsevier Inc. All rights reserved.
Background: Walking speed decreases in old age. Even though old adults regularly participate in exercise interventions, we do not know how the intervention-induced changes in physical abilities produce faster walking. The Potsdam Gait Study (POGS) will examine the effects of 10 weeks of power training and detraining on leg muscle power and, for the first time, on complete gait biomechanics, including joint kinematics, kinetics, and muscle activation in old adults with moderate mobility disability. Methods/Design: POGS is a randomized controlled trial with two arms, each crossed over, without blinding. Arm 1 starts with a 10-week control period to assess the reliability of the tests and is then crossed over to complete 25-30 training sessions over 10 weeks. Arm 2 completes 25-30 exercise sessions over 10 weeks, followed by a 10-week follow-up (detraining) period. The exercise program is designed to improve lower extremity muscle power. Main outcome measures are: muscle power, gait speed, and gait biomechanics measured at baseline and after 10 weeks of training and 10 weeks of detraining. Discussion: It is expected that power training will increase leg muscle power measured by the weight lifted and by dynamometry, and these increased abilities become expressed in joint powers measured during gait. Such favorably modified powers will underlie the increase in step length, leading ultimately to a faster walking speed. POGS will increase our basic understanding of the biomechanical mechanisms of how power training improves gait speed in old adults with moderate levels of mobility disabilities. (C) 2016 S. Karger AG, Basel
Theoretical models and preceding studies have described age-related alterations in neuronal activation of frontoparietal regions in a working memory (WM)load-dependent manner. However, to date, underlying neuronal mechanisms of these WM load-dependent activation changes in aging remain poorly understood. The aim of this study was to investigate these mechanisms in terms of effective connectivity by application of dynamic causal modeling with Bayesian Model Selection. Eighteen healthy younger (age: 20-32 years) and 32 older (60-75 years) participants performed an n-back task with 3 WM load levels during functional magnetic resonance imaging (fMRI). Behavioral and conventional fMRI results replicated age group by WM load interactions. Importantly, the analysis of effective connectivity derived from dynamic causal modeling, indicated an age-and performance-related reduction in WM load-dependent modulation of connectivity from dorsolateral prefrontal cortex to inferior parietal lobule. This finding provides evidence for the proposal that age-related WM decline manifests as deficient WM load-dependent modulation of neuronal top-down control and can integrate implications from theoretical models and previous studies of functional changes in the aging brain.
Objective: Fibroblast growth factor (FGF)21 is promptly induced by short fasting in animal models to regulate glucose and fat metabolism. Data on FGF21 in humans are inconsistent and FGF21 has not yet been investigated in old patients with cachexia, a complex syndrome characterized by inflammation and weight loss. The aim of this study was to explore the association of FGF21 with cachexia in old patients compared with their healthy counterparts. Methods: Serum FGF21 and its inactivating enzyme fibroblast activation protein (FAP)-cc were measured with enzyme-linked immunoassays. Cachexia was defined as >= 5% weight loss in the previous 3 mo and concurrent anorexia (Council on Nutrition appetite questionnaire). Results: We included 103 patients with and without cachexia (76.9 +/- 5.2 y of age) and 56 healthy controls (72.9 +/- 5.9 y of age). Cachexia was present in 16.5% of patients. These patients had significantly higher total FGF21 levels than controls (952.1 +/- 821.3 versus 525.2 +/- 560.3 pg/mL; P= 0.012) and the lowest FGF21 levels (293.3 +/- 150.9 pg/mL) were found in the control group (global P < 0.001). Although FAP-alpha did not differ between the three groups (global P = 0.082), bioactive FGF21 was significantly higher in patients with cachexia (global P = 0.002). Risk factor-adjusted regression analyses revealed a significant association between cachexia and total ((beta = 649.745 pg/mL; P < 0.001) and bioactive FGF21 (beta = 393.200 pg/mL; P <0.001), independent of sex, age, and body mass index. Conclusions: Patients with cachexia exhibited the highest FGF21 levels. Clarification is needed to determine whether this is an adaptive response to nutrient deprivation in disease-related cachexia or whether the increased FGF21 values contribute to the catabolic state. (C) 2018 Elsevier Inc. All rights reserved.
Methylglyoxal (MG), a highly reactive dicarbonyl, interacts with proteins to form advanced glycation end products (AGEs). AGEs include a variety of compounds which were shown to have damaging potential and to accumulate in the course of different conditions such as diabetes mellitus and aging. After confirming collagen as a main target for MG modifications in vivo within the extracellular matrix, we show here that MG-collagen disrupts fibroblast redox homeostasis and induces endoplasmic reticulum (ER) stress and apoptosis. In particular, MG-collagen-induced apoptosis is associated with the activation of the PERK-eIF2 alpha pathway and caspase-12. MG-collagen contributes to altered redox homeostasis by directly generating hydrogen peroxide and oxygen-derived free radicals. The induction of ER stress in human fibroblasts was confirmed using collagen extracts isolated from old mice in which MG-derived AGEs were enriched. In conclusion, MG-derived AGEs represent one factor contributing to diminished fibroblast function during aging.
Aging is a complex phenomenon that has detrimental effects on tissue homeostasis. The skeletal muscle is one of the earliest tissues to be affected and to manifest age-related changes such as functional impairment and the loss of mass. Common to these alterations and to most of tissues during aging is the disruption of the proteostasis network by detrimental changes in the ubiquitin-proteasomal system (UPS) and the autophagy-lysosomal system (ALS). In fact, during aging the accumulation of protein aggregates, a process mainly driven by increased levels of oxidative stress, has been observed, clearly demonstrating UPS and ALS dysregulation. Since the UPS and ALS are the two most important pathways for the removal of misfolded and aggregated proteins and also of damaged organelles, we provide here an overview on the current knowledge regarding the connection between the loss of proteostasis and skeletal muscle functional impairment and also how redox regulation can play a role during aging. Therefore, this review serves for a better understanding of skeletal muscle aging in regard to the loss of proteostasis and how redox regulation can impact its function and maintenance.
The skeletal muscle is a crucial tissue for maintaining whole body homeostasis. Aging seems to have a disruptive effect on skeletal muscle homeostasis including proteostasis. However, how aging specifically impacts slow and fast twitch fiber types remains elusive. Muscle proteostasis is largely maintained by the proteasomal system. Here we characterized the proteasomal system in two different fiber types, using a non-sarcopenic aging model. By analyzing the proteasomal activity and amount, as well as the polyubiquitinated proteins and the level of protein oxidation in Musculus soleus (Sol) and Musculus extensor digitorum longus (EDL), we found that the slow twitch Sol muscle shows an overall higher respiratory and proteasomal activity in young and old animals. However, especially during aging the fast twitch EDL muscle reduces protein oxidation by an increase of antioxidant capacity. Thus, under adaptive non-sarcopenic conditions, the two fibers types seem to have different strategies to avoid age-related changes.