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Sarcopenia and impairment in cognitive and physical performance.

ABSTRACT: Whether older adults with sarcopenia who underperform controls on tests of physical performance and cognition also have a higher likelihood of combined cognitive-physical impairment is not clear. We assessed the impact of sarcopenia on impairment in both aspects of functionality and the relative contribution of its components, muscle mass and strength.Two hundred and twenty-three community-dwelling adults aged 40 years and older (mean age =68.1±10.6 years; 65% female) were recruited and underwent physical functionality, anthropometry, and cognitive testing. Participants with low muscle mass were categorized as pre-sarcopenic; those with low muscle mass and muscle strength as sarcopenic; those with higher muscle mass and low muscle strength only were categorized as non-sarcopenic and were compared on risk of cognitive impairment (Montreal Cognitive Assessment <26; Ascertaining Dementia 8 ≥2), physical impairment (Mini Physical Performance Test <12), both, or neither by ordinal logistic regression.Compared to controls, those with sarcopenia were six times more likely to have combined cognitive impairment/physical impairment with a fully adjusted model showing a three-fold increased odds ratio. The results were consistent across different measures of global cognition (odds ratio =3.46, 95% confidence interval =1.07-11.45 for the Montreal Cognitive Assessment; odds ratio =3.61, 95% confidence interval =1.11-11.72 for Ascertaining Dementia 8). Pre-sarcopenic participants were not different from controls. The effect of sarcopenia on cognition is related to low muscle strength rather than low muscle mass.Individuals with sarcopenia are not only more likely to have single but also to have dual impairment in cognitive and physical function. Interventions designed to prevent sarcopenia and improve muscle strength may help reduce the burden of cognitive and physical impairments of functionality in community-dwelling seniors.

SUBMITTER: Tolea MI

PROVIDER: S-EPMC4388078 | biostudies-other | 2015

REPOSITORIES: biostudies-other

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Project description:BackgroundRecent evidence from cross-sectional and longitudinal studies supports the hypothesis that sarcopenia is associated with worsening cognitive function. However, primary evidence largely comes from high-income countries, whereas in low- and middle-income countries, this association has been underexplored. This study aimed to estimate the longitudinal association between sarcopenia and mild cognitive impairment in a sample of older Mexican adults.MethodsData come from the three waves of the World Health Organization (WHO) Study on Global AGEing and Adult Health (SAGE) in Mexico (2009, 2014, 2017). Four hundred ninety-six older adults, aged ≥50, were included. Sarcopenia was defined as having low muscle quantity and either/both slow gait speed and weak handgrip strength. Mild cognitive impairment was determined based on the recommendations of the National Institute on Aging-Alzheimer's Association. Cognitive function was evaluated by a composite cognitive score of five different cognitive tests: immediate and delayed recall, forward and backward digit span and semantic verbal fluency. Three-level mixed-effects models (logistic and linear) were used to estimate the longitudinal associations between sarcopenia, mild cognitive impairment and cognitive function.ResultsThe prevalence of mild cognitive impairment (8.9%, 12.9%, 16.0%) and sarcopenia (10.5%, 20.7%, 23.3%) showed a significant temporal increase for Waves 1, 2 and 3 (P-value < 0.01, respectively). The presence of sarcopenia was significantly associated with mild cognitive impairment (OR = 1.74; CI95% 1.02, 2.96; P = 0.04) and worse cognitive function (β = -0.57; CI95% -0.93, -0.21; P < 0.01). We observed significant associations between sarcopenia and immediate verbal recall (β = -0.14; CI95% -0.28, -0.01; P = 0.04), delayed verbal recall (β = -0.12; CI95% -0.23, -0.01; P = 0.03) and semantic verbal fluency (β = -0.17; CI95% -0.28, -0.05; P = 0.01). The prevalence of mild cognitive impairment increased at an annual rate of 0.8% for non-sarcopenic older adults, but nearly 1.5% for sarcopenic adults.ConclusionsSignificant longitudinal associations were observed between sarcopenia, mild cognitive impairment and cognitive function among older Mexican adults. Public health strategies, including policy research and clinical interventions, must be implemented in low- and middle-income countries in order to reduce or delay the onset of sarcopenia and thus improve population-level cognitive health among older adults.

Project description:Background: In the elderly, physical activity (PA) enhances cognitive performances, increases brain plasticity and improves brain health. The neurotrophic hypothesis is that the release of brain-derived neurotrophic factor (BDNF), which is implicated in brain plasticity and cognition, is triggered by PA because motoneurons secrete BDNF into the bloodstream during exercise. Individual differences in cognitive performance may be explained by individual differences in genetic predisposition. A single nucleotide polymorphism on the BDNF gene, BDNFVal66Met, affects activity-dependent BDNF secretion. This study investigated the influence of the BDNFVal66Met polymorphism on the relationship between PA and controlled inhibition performance in older adults. Methods: A total of 114 healthy elderly volunteers (mean age = 71.53 years old) were evaluated. Participants were genotyped for the BDNFVal66Met polymorphism. We evaluated inhibitory performance using choice reaction times (RT) and error rates from a Simon-like task and estimated their PA using two self-reported questionnaires. We established four groups according to PA level (active vs. inactive) and BDNFVal66Met genotype (Met carriers vs. Val-homozygous). The results were analyzed using ANOVA and ANCOVA, including age, gender and body mass index as covariates. Results: The BDNFVal66Met polymorphism interacted with PA on controlled inhibition performance. More specifically, inactive Val-homozygous participants exhibited a lower inhibition performance than active Val homozygotes and inactive Met carriers; the former had a higher error rate without differences in RT. Conclusion: Differences between individuals on inhibitory performance may be partially understood by the interaction between genetic influence in BDNF secretion and PA level. The results of this study clearly support the neurotrophic hypothesis that BDNF synthesis is an important mechanism underlying the influence of physical activity on brain structure and functions.

Project description:Background: Bridging scores generated from different cognitive assessment tools is necessary to efficiently track changes in cognition across the continuum of care. This study linked scores from the Montreal Cognitive Assessment-5 min (MoCA 5-min) to the interRAI cognitive Performance Scale (CPS), commonly adopted tools in clinical and long-term care settings, respectively. Methods: We included individual-level data from persons who participated in a home- and community-based care program for older people with mild impairment in Hong Kong. The program used the interRAI-Check Up instrument for needs assessment and service matching between 2017 and 2020. Each participant's cognitive performance was assessed using CPS, CPS Version 2 (CPS2), and MoCA 5-min. We performed equipercentile linking with bivariate log-linear smoothing to establish equivalent scores between the two scales. Results: 3,543 participants had valid data on both scales; 66% were female and their average age was 78.9 years (SD = 8.2). The mean scores for MoCA 5-min, CPS, and CPS2 were 18.5 (SD = 5.9), 0.7 (SD = 0.7), and 1.3 (SD = 1.1), respectively. A CPS or CPS2 score of 0 (intact cognition) corresponds to MoCA 5-min scores of 24 and 25, respectively. At the higher end, a CPS score of 3 (moderately impaired) and a CPS2 score of 5 (moderately impaired Level-2) corresponded to MoCA 5-min scores of 0 and 1, respectively. The linking functions revealed the floor and ceiling effects that exist for the different scales, with CPS and CPS2 measuring more-severe cognitive impairment while the MoCA 5-min was better suited to measure mild impairment. Conclusions: We provided score conversions between MoCA 5-min and CPS/CPS2 within a large cohort of Hong Kong older adults with mild physical or cognitive impairment. This enabled continuity in repeated assessment with different tools and improved comparability of cognitive scores generated from different tools from diverse populations and research cohorts.

Project description:The Short Physical Performance Battery (SPPB) is a widely accepted test for measuring lower extremity function in older adults. However, there are concerns regarding the examination time required to conduct a complete SPPB consisting of three components (walking speed, chair rise, and standing balance tests) in clinical settings. We aimed to assess specific examination times for each component of the electronic Short Physical Performance Battery (eSPPB) and compare the ability of the original three-component examinations (eSPPB) and a faster, two-component examination without a balance test (electronic Quick Physical Performance Battery, eQPPB) to classify sarcopenia. The study was a retrospective, cross-sectional study which included 124 ambulatory outpatients who underwent physical performance examination at a geriatric clinic of a tertiary, academic hospital in Seoul, Korea, between December 2020 and March 2021. For eSPPB, we used a toolkit containing sensors and software (Dyphi, Daejeon, Korea) developed to measure standing balance, walking speed, and chair rise test results. Component-specific time stamps were used to log the raw data. Duration of balance examination, 5 times sit-to-stand test (5XSST), and walking speed examination were calculated. Sarcopenia was determined using the 2019 Asian Working Group for Sarcopenia (AWGS) guideline. The median age was 78 years (interquartile range, IQR: 73,82) and 77 subjects (62.1%) were female. The total mean eSPPB test time was 124.8 ± 29.0 s (balance test time 61.8 ± 12.3 s, 49.5%; gait speed test time 34.3 ± 11.9 s, 27.5%; and 5XSST time 28.7 ± 19.1 s, 23.0%). The total mean eQPPB test time was 63.0 ± 25.4 s. Based on the AWGS criteria, 34 (27.4%) patient's results were consistent with sarcopenia. C-statistics for classifying sarcopenia were 0.83 for eSPPB and 0.85 for eQPPB (p = 0.264), while eQPPB took 49.5% less measurement time compared with eSPPB. Breakdowns of eSPPB test times were identified. Omitting balance tests may reduce test time without significantly affecting the classifying ability of eSPPB for sarcopenia.

Project description:Physical frailty and impaired cognition are common in patients with cirrhosis. Physical frailty can be assessed using performance-based tests, but the extent to which impaired cognition may impact performance is not well characterized. We assessed the relationship between impaired cognition and physical frailty in patients with cirrhosis. We enrolled 1,623 ambulatory adult patients with cirrhosis waiting for liver transplantation at 10 sites. Frailty was assessed with the liver frailty index (LFI; "frail," LFI ≥ 4.4). Cognition was assessed at the same visit with the number connection test (NCT); continuous "impaired cognition" was examined in primary analysis, with longer NCT (more seconds) indicating worse impaired cognition. For descriptive statistics, "impaired cognition" was NCT ≥ 45 seconds. Linear regression associated frailty and impaired cognition; competing risk regression estimated subhazard ratios (sHRs) of wait-list mortality (i.e., death/delisting for sickness). Median NCT was 41 seconds, and 42% had impaired cognition. Median LFI (4.2 vs. 3.8) and rates of frailty (38% vs. 20%) differed between those with and without impaired cognition. In adjusted analysis, every 10-second NCT increase associated with a 0.08-LFI increase (95% confidence interval [CI], 0.07-0.10). In univariable analysis, both frailty (sHR, 1.63; 95% CI, 1.43-1.87) and impaired cognition (sHR, 1.07; 95% CI, 1.04-1.10) associated with wait-list mortality. After adjustment, frailty but not impaired cognition remained significantly associated with wait-list mortality (sHR, 1.55; 95% CI, 1.33-1.79). Impaired cognition mediated 7.4% (95% CI, 2.0%-16.4%) of the total effect of frailty on 1-year wait-list mortality. Conclusion: Patients with cirrhosis with higher impaired cognition displayed higher rates of physical frailty, yet frailty independently associated with wait-list mortality while impaired cognition did not. Our data provide evidence for using the LFI to understand mortality risk in patients with cirrhosis, even when concurrent impaired cognition varies.

Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Keywords: Immediate Early Genes, Insulin Signaling, Cholesterol, Myelination, Glia, Inflammation, Young and Old comparaison, behavioral-characterization, Aging-related cognitive impairment.

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Sarcopenia and impairment in cognitive and physical performance.

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