Balance control interferes with the tracing performance of a pattern with mirror-reversed vision in older persons

GeroScience - When tracing a template with mirror-reversed vision (or distorted vision), the sensory information arising from the movement does not match the expected sensory consequences. In such...     

The dynamic relationship between cognitive function and walking speed: the English Longitudinal Study of Ageing

Cognitive deficiency and oxidative stress have been well documented in aging and in neurodegenerative disorders such as Alzheimer’s disease. In this study, we assessed the therapeutic effect of polyprenols on d-galactose-induced cognitive impairment in mice by testing on of behavioral and cognitive performance. In order to explore the possible role of polyprenols against d-galactose-induced oxidative damages, we assessed various biochemical indicators. Chronic administration of d-galactose (150 mg/kg·d, s.c.) for 7 weeks significantly impaired cognitive performance (both in step-through passive and active avoidance tests) and locomotor activity (in open-field test) and the ability of spatial learning and memory (in Morris water maze test) compared with the control group. The results revealed that polyprenols treatment for 2 weeks significantly ameliorated model mice’s cognitive performance and oxidative defense. All groups of polyprenols enhanced the learning and memory ability in step-through passive and active avoidance tests, locomotor activity in open-field test, and the ability of spatial learning and memory in Morris water maze test. Furthermore, high and middle level of polyprenols significantly increased total antioxidative capacity (T-AOC), glutathione peroxidase (GSH-Px), super oxide dismutase (SOD) activity, neprilysin (NEP), and β-site AβPP cleaving enzyme 1 (BACE1) expression, while nitric oxide (NO), nitric oxide synthase (NOS) activity, malondialdehyde (MDA) concentration, and the level of Aβ1-42 and presenilin 1 (PS1) were decreased. Polyprenols have a significant relieving effect on learning, memory, and spontaneous activities in a d-galactose-induced mouse model and ameliorates cognitive impairment and biochemical dysfunction in mice. In summary, we have demonstrated that polyprenols may ameliorate memory and cognitive impairment via enhancing oxidative defense and affecting generation and dissimilation of Aβ-related enzymes, suggesting that polyprenols represent a novel drug for treating Alzheimer’s disease.     

A mechanistic model of mismatch negativity in the ageing brain

ObjectiveWe investigated the neurophysiological mechanisms underpinning the generation of the mismatch negativity (MMN) in the ageing brain.MethodsWe used dynamic causal modelling (DCM) to study connectivity models for healthy young and old subjects. MMN was elicited with an auditory odd-ball paradigm in two groups of healthy subjects with mean age 74 (n = 30) and 26 (n = 26). DCM was implemented using up to five cortical nodes. We tested models with different hierarchical complexities.ResultsWe showed that the network generating MMN consisted of 5 nodes that could modulate all intra- and inter-nodal connections. The inversion of this model showed that old subjects had increased input from rSTG to the rIFG (p < 0.01) together with increased inhibition of pyramidal cells (p < 0.05). Furthermore, there was reduced modulation of activity within rIFG (p < 0.02) on stimulus change.ConclusionThe age related change in MMN is due to a decline in frontal-based control mechanisms, with alterations in connectivity between temporal and frontal regions together with a dysregulation of the excitatory–inhibitory balance in the rIFG.SignificanceThis study provides for the first time a neurobiological explanation for the age related changes of the MMN in the ageing brain.     

Mitophagy Receptors and Mediators: Therapeutic Targets in the Management of Cardiovascular Ageing

Mitophagy serves as a cardinal regulator in the maintenance of mitochondrial integrity, function, and cardiovascular homeostasis, through the fine control and governance of cellular metabolism, ATP production, redox balance, and mitochondrial quality and quantity control. As a unique form of selective autophagy, mitophagy specifically recognizes and engulfs long-lived or damaged (depolarized) mitochondria through formation of the double-membraned intracellular organelles - mitophagosomes, ultimately resulting in lysosomal degradation. Levels of mitophagy are reported to be altered in pathological settings including cardiovascular diseases and biological ageing although the precise nature of mitophagy change in ageing and ageing-associated cardiovascular deterioration remains poorly defined. Ample clinical and experimental evidence has depicted a convincing tie between cardiovascular ageing and altered mitophagy. In particular, ageing perturbs multiple enigmatic various signal machineries governing mitophagy, mitochondrial quality, and mitochondrial function, contributing to ageing-elicited anomalies in the cardiovascular system. This review will update novel regulatory mechanisms of mitophagy especially in the perspective of advanced ageing, and discuss how mitophagy dysregulation may be linked to cardiovascular abnormalities in ageing. We hope to pave the way for development of new therapeutic strategies against the growing health and socieconomical issue of cardiovascular ageing through targeting mitophagy.     

Age and gender,two key factors in the associations between physical activity and strength during the ageing process

Objectives

The aims of this study were to identify if the associations of physical activity (PA) and muscle strength may vary throughout the ageing process; to study the differences among genders in the relationships between PA and strength in elderly people and to test whether these differences are explained by the hormonal, nutritional and inflammatory status.

Study design

A total of 1741 people ≥65 years of age participated in this cross-sectional study.

Main outcome measures

Upper- and lower-limbs maximal voluntary isometric strength was obtained using standardized techniques and equipment. PA was recorded by a validated questionnaire. The associations of PA with strength were assessed using generalized linear regression models with a Gamma-distributed dependent variable.

Results

A significant gender by PA interaction was found for all strength-related variables (all P < 0.01). Moreover, when sexual hormones, albumin or C-Reactive protein were taken into account in the model, the results did not significantly change. In women, PA was positively associated with upper and lower-body strength; however in men, PA was only associated with grip and knee strength (both P < 0.01). Higher strength values were associated with higher levels of PA, especially in women. However, this tendency had a different pattern across the age range, showing a stronger association in the ‘young’ elderly compared with the ‘old’ elderly.

Conclusion

Higher levels of PA are related to greater muscle strength, especially in women and those who were younger.     

Role of translation initiation factor 4G in lifespan regulation and age-related health

Inhibiting expression of eukaryotic translation initiation factor 4G (eIF4G) arrests normal development but extends lifespan when suppressed during adulthood. In addition to reducing overall translation, inhibition alters the stoichiometry of mRNA translation in favor of genes important for responding to stress and against those associated with growth and reproduction in C. elegans. In humans, aberrant expression of eIF4G is associated with certain forms of cancer and neurodegeneration. Here we review what is known about the roles of eIF4G in molecular, cellular, and organismal contexts. Also discussed are the gaps in understanding of this factor, particularly with regard to the roles of specific forms of expression in individual tissues and the importance of understanding eIF4G for development of potential therapeutic applications.     

Sleep and brain morphological changes in the eighth decade of life

ObjectiveSleep is important for brain health. We analysed associations between usual sleep habits and magnetic resonance imaging (MRI) markers of neurodegeneration (brain atrophy), vascular damage (white matter hyperintensities, WMH) and waste clearance (perivascular spaces, PVS) in older community-dwelling adults.MethodWe collected self-reported usual sleep duration, quality and medical histories from the Lothian Birth Cohort 1936 (LBC1936) age 76 years and performed brain MRI. We calculated sleep efficiency, measured WMH and brain volumes, quantified PVS, and assessed associations between sleep measures and brain markers in multivariate models adjusted for demographic and medical history variables.ResultsIn 457 subjects (53% males, mean age 76 ± 0.65 years), we found: brain and white matter loss with increased weekend daytime sleep (β = −0.114, P = 0.03; β = −0.122, P = 0.007 respectively), white matter loss with less efficient sleep (β = 0.132, P = 0.011) and PVS increased with interrupted sleep (OR 1.84 95% CI, P = 0.025).ConclusionCross-sectional associations of sleep parameters with brain atrophy and more PVS suggest adverse relationships between usual sleep habits and brain health in older people that should be evaluated longitudinally.