scholarly journals Social isolation and the aging brain. Social isolation is linked to declining grey matter structure and cognitive functions in the LIFE-Adult panel study

2021 ◽  
Author(s):  
Laurenz Lammer ◽  
Frauke Beyer ◽  
Melanie Luppa ◽  
Christian Sander ◽  
Ronny Baber ◽  
...  
Keyword(s):  
Social Isolation ◽  
Cortical Thickness ◽  
Cognitive Functions ◽  
Grey Matter ◽  
Brain Aging ◽  
Panel Study ◽  
Hippocampal Volume ◽  
Cortical Atrophy ◽  
Aging Brain ◽  
The Impact

Background Social isolation is a risk factor for dementia, a devastating disease with a rapidly growing global prevalence. However, the link between social isolation and changes in brain structure and function is poorly understood, as studies are scarce in number, methodologically inconsistent and small in size. In this pre-registered analysis of a large population-based panel study, we aimed to determine the impact of social isolation on brain structures and cognitive functions central to age associated decline and dementia. Methods and findings We analysed data of 1992 cognitively healthy participants of the LIFE-Adult study at baseline (age range: 50-82 years) and of 1409 particpants at follow-up (average change in age: 5.89 years). We measured social isolation using the 30-point Lubben Social Network Scale (LSNS) and derived measures of grey matter structure from anatomical 3T MRIs. We employed covariate adjusted linear mixed models to test the associations of baseline social isolation and change in social isolation with hippocampal volume, cognitive functions (executive functions, memory, processing speed) and cortical thickness. We found stronger baseline social isolation to be significantly associated with smaller hippocampal volumes (β = −5.5 mm3/LSNS point(pt), FDR q = 0.004, BF = 14.6) and lower cognitive functions (all β < −0.014 SD/pt, FDR q < 0.003, BF > 49). Increases in social isolation over time were linked to hippocampal volume decline (β = −4.9 mm3/pt, FDR q = 0.01, BF = 2.9) and worse memory performance (β = −0.013 SD/pt, FDR q = 0.04, BF = 1.1). Furthermore, we detected a significant interaction of baseline social isolation with change in age on hippocampal volume (β = −0.556 mm3/pt*a, q = 0.04, BF = 0.5), indicating accelerated brain aging in more isolated individuals. Moreover, social isolation cross-sectionally and longitudinally correlated with lower cortical thickness in multiple clusters in the orbitofrontal cortex, precuneus and other areas (FDR q < 0.05). Conclusions Here, we provide evidence that social isolation contributes to hippocampal and cortical atrophy and subtle cognitive decline in non-demented mid- to late-life adults. Importantly, within-subject effects of social isolation were similar to between-subject effects, indicating an opportunity for targeting social isolation to reduce dementia risk.

scholarly journals Joint contributions of cortical morphometry and white matter microstructure in healthy brain aging: A partial least squares correlation analysis

2019 ◽  
Author(s):  
David A. Hoagey ◽  
Jenny R. Rieck ◽  
Karen M. Rodrigue ◽  
Kristen M. Kennedy
Keyword(s):  
White Matter ◽  
Least Squares ◽  
Surface Area ◽  
Partial Least Squares ◽  
Cortical Thickness ◽  
Brain Aging ◽  
Univariate Analysis ◽  
Tissue Type ◽  
Cortical Atrophy ◽  
Multivariate Techniques

AbstractCortical atrophy and degraded axonal health have been shown to coincide during normal aging; however, few studies have examined these measures together. To lend insight into both the regional specificity and the relative timecourse of structural degradation of these tissue compartments across the lifespan, we analyzed grey matter (GM) morphometry (cortical thickness, surface area, volume) and estimates of white matter (WM) microstructure (fractional anisotropy, mean diffusivity) using traditional univariate and more robust multivariate techniques to examine age associations in 186 healthy adults aged 20-94 years old. Univariate analysis of each tissue type revealed that negative age associations were largest in frontal grey and white matter tissue and weaker in temporal, cingulate, and occipital regions, representative of not only an anterior-to-posterior gradient, but also a medial-to-lateral gradient. Multivariate partial least squares correlation (PLSC) found the greatest covariance between GM and WM was driven by the relationship between WM metrics in the anterior corpus callosum and projections of the genu, anterior cingulum, and fornix; and with GM thickness in parietal and frontal regions. Surface area was far less susceptible to age effects and displayed less covariance with WM metrics, while regional volume covariance patterns largely mirrored those of cortical thickness. Results support a retrogenesis-like model of aging, revealing a coupled relationship between frontal and parietal GM and the underlying WM, which evidence the most protracted development and the most vulnerability during healthy aging.

COVID-19 in German Nursing Homes: A Panel Study on Morbidity, Burden of Care, and Social Isolation

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 407-408
Author(s):  
Kathrin Seibert ◽  
Dominik Domhoff ◽  
Franziska Heinze ◽  
Benedikt Preuss ◽  
Heinz Rothgang ◽  
...  
Keyword(s):  
Nursing Homes ◽  
Social Isolation ◽  
Online Survey ◽  
Panel Study ◽  
Protective Equipment ◽  
Burden Of Care ◽  
Care Needs ◽  
Morbidity Burden ◽  
The Impact ◽  
Second Wave

Abstract Germany was hit by the second wave of the pandemic much harder than by the first wave. The study aims to describe the extent to which nursing homes (NH) are affected by COVID-19. About 8,000 NHs were invited to participate in two waves of an online survey, with a share of 5-10% participating. The share of all deceased NH-residents with COVID-19 is about 50% (04/2020-02/2021). Factors that increase the risk of an outbreak in NH are the spread of the virus in the population, the size of the institution and staff-resident-ratio. The initial lack of protective equipment has decreased during the second wave, but the facilities have to cope with massive additional care needs with reduced staff. NHs have partly banned contacts between residents and relatives. As a conclusion the support of NH in their attempt to fight the impact of this and further pandemic situations requires highest attention.

The impact of localized grey matter damage on neighboring connectivity: posterior cortical atrophy and the visual network

2018 ◽  
Vol 13 (5) ◽  
pp. 1292-1301 ◽  
Author(s):  
Haya Glick-Shames ◽  
Yael Backner ◽  
Atira Bick ◽  
Noa Raz ◽  
Netta Levin
Keyword(s):  
Grey Matter ◽  
Cortical Atrophy ◽  
Posterior Cortical Atrophy ◽  
The Impact ◽  
Visual Network

scholarly journals Brain aging-dependent glioma traits reversible by NAD+/BDNF-mediated neuronal reactivation

2020 ◽  
Author(s):  
Daisuke Yamashita ◽  
Victoria L Flanary ◽  
Rachel B Munk ◽  
Kazuhiro Sonomura ◽  
Saya Ozaki ◽  
...  
Keyword(s):  
Brain Aging ◽  
Tumor Burden ◽  
Synaptic Activity ◽  
Aging Brain ◽  
Neuronal Signaling ◽  
Nicotinamide Mononucleotide ◽  
Brain Responses ◽  
Phenotypic Reversal ◽  
The Impact ◽  
Old Mice

SummaryThe rise in aging population worldwide is increasing death from cancer, including glioblastoma. Here, we explore the impact of brain aging on glioma tumorigenesis. We find that glioblastoma in older patients and older mice displayed reduced neuronal signaling, including a decline of NTRK-like family member 6 (SLITRK6), a receptor for neurotrophic factor BDNF. This reduction was linked to the systemic decline of nicotinamide adenine dinucleotide (NAD+) with aging, as old mice exposed to young blood via parabiosis or supplemented with the NAD+ precursor NMN (nicotinamide mononucleotide) reverted phenotypically to young-brain responses to glioma, with reactivated neuronal signaling and reduced death from tumor burden. Interestingly, the phenotypic reversal by NMN was largely absent in old mice undergoing parabiosis with BDNF+/- young mice and in BDNF+/- mice undergoing tumor challenge, supporting the notion that the lower NAD+-BDNF signaling in the aging brain aggravated glioma tumorigenesis. We propose that the aging-associated decline in brain NAD+ worsens glioma outcomes at least in part by decreasing neuronal/synaptic activity and increasing neuroinflammation.

scholarly journals Higher VO2max is associated with thicker cortex and lower grey matter blood flow in older adults

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gaia Olivo ◽  
Jonna Nilsson ◽  
Benjamín Garzón ◽  
Alexander Lebedev ◽  
Anders Wåhlin ◽  
...  
Keyword(s):  
Older Adults ◽  
Blood Flow ◽  
Physical Exercise ◽  
Cortical Thickness ◽  
Grey Matter ◽  
Brain Activity ◽  
Moderate Intensity ◽  
Grey Matter Volume ◽  
Matter Volume ◽  
The Impact

AbstractVO2max (maximal oxygen consumption), a validated measure of aerobic fitness, has been associated with better cerebral artery compliance and measures of brain morphology, such as higher cortical thickness (CT) in frontal, temporal and cingular cortices, and larger grey matter volume (GMV) of the middle temporal gyrus, hippocampus, orbitofrontal cortex and cingulate cortex. Single sessions of physical exercise can promptly enhance cognitive performance and brain activity during executive tasks. However, the immediate effects of exercise on macro-scale properties of the brain’s grey matter remain unclear. We investigated the impact of one session of moderate-intensity physical exercise, compared with rest, on grey matter volume, cortical thickness, working memory performance, and task-related brain activity in older adults. Cross-sectional associations between brain measures and VO2max were also tested. Exercise did not induce statistically significant changes in brain activity, grey matter volume, or cortical thickness. Cardiovascular fitness, measured by VO2max, was associated with lower grey matter blood flow in the left hippocampus and thicker cortex in the left superior temporal gyrus. Cortical thickness was reduced at post-test independent of exercise/rest. Our findings support that (1) fitter individuals may need lower grey matter blood flow to meet metabolic oxygen demand, and (2) have thicker cortex.

scholarly journals Diet modulates brain network stability, a biomarker for brain aging, in young adults

2020 ◽  
Vol 117 (11) ◽  
pp. 6170-6177 ◽  
Author(s):  
Lilianne R. Mujica-Parodi ◽  
Anar Amgalan ◽  
Syed Fahad Sultan ◽  
Botond Antal ◽  
Xiaofei Sun ◽  
...  
Keyword(s):  
Ketogenic Diet ◽  
Large Scale ◽  
Brain Aging ◽  
Brain Network ◽  
Detection Sensitivity ◽  
Aging Brain ◽  
Standard Diet ◽  
Network Stability ◽  
The Impact ◽  
Ketone Ester

Epidemiological studies suggest that insulin resistance accelerates progression of age-based cognitive impairment, which neuroimaging has linked to brain glucose hypometabolism. As cellular inputs, ketones increase Gibbs free energy change for ATP by 27% compared to glucose. Here we test whether dietary changes are capable of modulating sustained functional communication between brain regions (network stability) by changing their predominant dietary fuel from glucose to ketones. We first established network stability as a biomarker for brain aging using two large-scale (n= 292, ages 20 to 85 y;n= 636, ages 18 to 88 y) 3 T functional MRI (fMRI) datasets. To determine whether diet can influence brain network stability, we additionally scanned 42 adults, age < 50 y, using ultrahigh-field (7 T) ultrafast (802 ms) fMRI optimized for single-participant-level detection sensitivity. One cohort was scanned under standard diet, overnight fasting, and ketogenic diet conditions. To isolate the impact of fuel type, an independent overnight fasted cohort was scanned before and after administration of a calorie-matched glucose and exogenous ketone ester (d-β-hydroxybutyrate) bolus. Across the life span, brain network destabilization correlated with decreased brain activity and cognitive acuity. Effects emerged at 47 y, with the most rapid degeneration occurring at 60 y. Networks were destabilized by glucose and stabilized by ketones, irrespective of whether ketosis was achieved with a ketogenic diet or exogenous ketone ester. Together, our results suggest that brain network destabilization may reflect early signs of hypometabolism, associated with dementia. Dietary interventions resulting in ketone utilization increase available energy and thus may show potential in protecting the aging brain.

scholarly journals Searching for replicable associations between cortical thickness and psychometric variables in healthy adults: empirical facts

2020 ◽  
Author(s):  
Shahrzad Kharabian Masouleh ◽  
Simon B. Eickhoff ◽  
Sarah Genon
Keyword(s):  
Cortical Thickness ◽  
Grey Matter ◽  
Healthy Adults ◽  
Effect Sizes ◽  
Grey Matter Volume ◽  
Scientific Communities ◽  
The Public ◽  
Psychometric Data ◽  
Extended Range ◽  
The Impact

AbstractThe study of associations between inter-individual differences in brain structure and behaviour has a long history in psychology and neuroscience. Many associations between psychometric data, particularly intelligence and personality measures and local variations of brain cortical thickness (CT) have been reported. While the impact of such findings often go beyond scientific communities, resonating in the public mind, their replicability is rarely evidenced.Here, we empirically investigated the replicability of associations of an extended range of psychometric variables and CT in a large cohort of healthy adults. Our analyses revealed low likelihood of significant associations. Furthermore, significant associations from exploratory analyses showed overestimated effect sizes and were rarely replicable in an independent sample.We discuss the interpretation and implications of these findings within the context of accumulating evidence of the poor replicability of structural-brain-behaviour associations using grey matter volume, and more broadly of the replicability crisis of brain and behaviour sciences.

P2-434: Longitudinal changes in grey matter volumes and cortical thickness in Posterior Cortical Atrophy

2010 ◽  
Vol 6 ◽  
pp. S446-S447
Author(s):  
Manja Lehmann ◽  
Josephine Barnes ◽  
Gerard R. Ridgway ◽  
Elizabeth K. Warrington ◽  
Nick C. Fox ◽  
...  
Keyword(s):  
Cortical Thickness ◽  
Grey Matter ◽  
Cortical Atrophy ◽  
Posterior Cortical Atrophy ◽  
Longitudinal Changes

scholarly journals Reaction-Diffusion Model of Cortical Atrophy Spread during Early Stages of Alzheimer’s Disease

2020 ◽  
Author(s):  
Sue Kulason ◽  
Michael I Miller ◽  
Alain Trouvé ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Diffusion Model ◽  
Cortical Thickness ◽  
Grey Matter ◽  
Reaction Diffusion ◽  
Cortical Atrophy ◽  
Early Stages ◽  
Reaction Diffusion Model ◽  
Rhinal Cortex

1.AbstractThis study introduces a reaction-diffusion model of atrophy spread across the rhinal cortex during early stages of Alzheimer’s disease. Our finite elements model of atrophy spread is motivated by histological evidence of a spatio-temporally specific pattern of neurofibrillary tau accumulation, and evidence of grey matter atrophy correlating with sites of neurofibrillary tau accumulation. The goal is to estimate disease-related parameters such as the origin of atrophy, the speed at which atrophy spreads, and the stage of the disease. We solve a constrained optimization problem using the adjoint state method and gradient descent to match modeled cortical thickness to observed cortical thickness as calculated from 3T MRI scans. Simulation testing shows that disease-related parameters can be estimated accurately with as little as 2 years of annual observations, depending on the stage of the disease. Case studies of 3 subjects suggests that we can pinpoint the origin of atrophy to the anterior transentorhinal cortex, and that the speed of atrophy spread is less than 1 mm per year. In the future, this type of modeling could be useful to stage the progression of the disease prior to the onset of clinical symptoms.2.Author SummaryMisfolded tau proteins are associated with Alzheimer’s disease. They are known to accumulate and spread across the rhinal cortex, which is an area of the temporal lobe. Recent imaging studies suggest that we can detect grey matter thinning that occurs in pattern similar to tau spread. In this study, we introduce a model of disease spread to examine where thinning begins, how fast it spreads, and the stage of the disease. The results show that the origin of thinning corresponds with the earliest known location of tau accumulation, and spreads at a rate of less than 1 mm per year. Future work may focus on staging the progression of the disease using this type of model.

The Need to Belong and the Relationship Between Loneliness and Health

2014 ◽  
Vol 22 (4) ◽  
pp. 194-201 ◽  
Author(s):  
Freda-Marie Hartung ◽  
Britta Renner
Keyword(s):  
Individual Differences ◽  
Social Isolation ◽  
Social Situation ◽  
First Year ◽  
Health State ◽  
Need To Belong ◽  
First Year University ◽  
Perceived Social Isolation ◽  
The Impact ◽  
The Relationship

Humans are social animals; consequently, a lack of social ties affects individuals’ health negatively. However, the desire to belong differs between individuals, raising the question of whether individual differences in the need to belong moderate the impact of perceived social isolation on health. In the present study, 77 first-year university students rated their loneliness and health every 6 weeks for 18 weeks. Individual differences in the need to belong were found to moderate the relationship between loneliness and current health state. Specifically, lonely students with a high need to belong reported more days of illness than those with a low need to belong. In contrast, the strength of the need to belong had no effect on students who did not feel lonely. Thus, people who have a strong need to belong appear to suffer from loneliness and become ill more often, whereas people with a weak need to belong appear to stand loneliness better and are comparatively healthy. The study implies that social isolation does not impact all individuals identically; instead, the fit between the social situation and an individual’s need appears to be crucial for an individual’s functioning.

Sign in / Sign up

Export Citation Format

Share Document