We present a first-principles lattice QCD+QED calculation at physical pion mass of the leading-order hadronic vacuum polarization contribution to the muon anomalous magnetic moment. The total ...contribution of up, down, strange, and charm quarks including QED and strong isospin breaking effects is a_{μ}^{HVP LO}=715.4(18.7)×10^{-10}. By supplementing lattice data for very short and long distances with R-ratio data, we significantly improve the precision to a_{μ}^{HVP LO}=692.5(2.7)×10^{-10}. This is the currently most precise determination of a_{μ}^{HVP LO}.
We report the first lattice QCD calculation of the hadronic vacuum polarization (HVP) disconnected contribution to the muon anomalous magnetic moment at physical pion mass. The calculation uses a ...refined noise-reduction technique that enables the control of statistical uncertainties at the desired level with modest computational effort. Measurements were performed on the 48^{3}×96 physical-pion-mass lattice generated by the RBC and UKQCD Collaborations. We find the leading-order hadronic vacuum polarization a_{μ}^{HVP(LO)disc}=-9.6(3.3)(2.3)×10^{-10}, where the first error is statistical and the second systematic.
Studies examining the link between objective measures of total daily physical activity and incident Alzheimer disease (AD) are lacking. We tested the hypothesis that an objective measure of total ...daily physical activity predicts incident AD and cognitive decline.
Total daily exercise and nonexercise physical activity was measured continuously for up to 10 days with actigraphy (Actical®; Philips Healthcare, Bend, OR) from 716 older individuals without dementia participating in the Rush Memory and Aging Project, a prospective, observational cohort study. All participants underwent structured annual clinical examination including a battery of 19 cognitive tests.
During an average follow-up of about 4 years, 71 subjects developed clinical AD. In a Cox proportional hazards model adjusting for age, sex, and education, total daily physical activity was associated with incident AD (hazard ratio = 0.477; 95% confidence interval 0.273-0.832). The association remained after adjusting for self-report physical, social, and cognitive activities, as well as current level of motor function, depressive symptoms, chronic health conditions, and APOE allele status. In a linear mixed-effect model, the level of total daily physical activity was associated with the rate of global cognitive decline (estimate 0.033, SE 0.012, p = 0.007).
A higher level of total daily physical activity is associated with a reduced risk of AD.
We present results for several light hadronic quantities (f sub(pi), f sub(K), B sub(K), m sub(ud), m sub(s), t super(1/2) sub(0), w sub(0)) obtained from simulations of 2+1 flavor domain wall ...lattice QCD with large physical volumes and nearly physical pion masses at two lattice spacings. We perform a short, O(3)%, extrapolation in pion mass to the physical values by combining our new data in a simultaneous chiral/continuum "global fit" with a number of other ensembles with heavier pion masses. We use the physical values of m sub(pi), m sub(K) and m sub(Omega) to determine the two quark masses and the scale-all other quantities are outputs from our simulations. We obtain results with subpercent statistical errors and negligible chiral and finite-volume systematics for these light hadronic quantities, including f sub(pi)=130.2(9)MeV; f sub(K)=155.5(8)MeV; the average up/down quark mass and strange quark mass in the MS scheme at 3 GeV, 2.997(49) and 81.64(1.17) MeV respectively; and the neutral kaon mixing parameter, BK, in the renormalization group invariant scheme, 0.750(15) and the MS scheme at 3 GeV, 0.530(11).
We present a lattice QCD calculation of the ΔI = 1/2, K → π π decay amplitude A 0 and ϵ ′, the measure of direct C P violation in K → π π decay, improving our 2015 calculation 1 of these quantities. ...Both calculations were performed with physical kinematics on a 323 × 64 lattice with an inverse lattice spacing of a−1 = 1.3784(68) GeV . However, the current calculation includes nearly 4 times the statistics and numerous technical improvements allowing us to more reliably isolate the π π ground state and more accurately relate the lattice operators to those defined in the standard model. We find Re(A0) = 2.99(0.32)(0.59) × 10−7 GeV and Im(A0) = − 6.98(0.62)(1.44) × 10−11 GeV, where the errors are statistical and systematic, respectively. The former agrees well with the experimental result Re(A0) = 3.3201(18) × 10−7 GeV . These results for A0 can be combined with our earlier lattice calculation of A2 2 to obtain Re(ϵ′/ϵ) = 21.7(2.6)(6.2)(5.0) × 10−4, where the third error represents omitted isospin breaking effects, and Re(A0) / Re(A2) = 19.9(2.3)(4.4). The first agrees well with the experimental result of Re(ϵ′/ϵ) = 16.6(2.3) × 10−4. A comparison of the second with the observed ratio Re(A0) / Re(A2) = 22.45(6), demonstrates the standard model origin of this " ΔI = 1/2 rule" enhancement.
To test the cognitive dedifferentiation hypothesis that cognitive abilities become increasingly correlated in late life.
Participants are 174 older persons without dementia at the beginning of a ...longitudinal clinical-pathologic cohort study. At annual intervals for 6 to 15 years prior to death, they completed a battery of cognitive performance tests from which previously established composite measures of episodic memory, semantic memory, working memory, and perceptual speed were derived. At death, there was a uniform neuropathologic assessment and levels of diffuse plaques, neuritic plaques, and neurofibrillary tangles were summarized in a composite measure. Change in the 4 cognitive outcomes was analyzed simultaneously in a mixed-effects model that allowed rate of decline to accelerate at a variable point before death.
On average, cognitive decline before the terminal period was relatively gradual, and rates of change in different cognitive domains were moderately correlated, ranging from 0.25 (episodic memory-working memory) to 0.46 (episodic memory-semantic memory). By contrast, cognition declined rapidly during the terminal period, and rates of change in different cognitive functions were strongly correlated, ranging from 0.83 (working memory-perceptual speed) to 0.89 (episodic memory-semantic memory, semantic memory-working memory). Higher level of plaques and tangles on postmortem examination was associated with faster preterminal decline and earlier onset of terminal decline but not with rate of terminal decline or correlations between rates of change in different cognitive functions.
In the last years of life, covariation among cognitive abilities sharply increases consistent with the cognitive dedifferentiation hypothesis.
Lewy bodies are common in the ageing brain and often co-occur with Alzheimer's disease pathology. There is little known regarding the independent role of Lewy body pathology in cognition impairment, ...decline and fluctuations in community-dwelling older persons. We examined the contribution of Lewy body pathology to dementia, global cognition, cognitive domains, cognitive decline and fluctuations in 872 autopsied subjects (mean age = 87.9 years) from the Rush Religious Order Study (n = 491) and Memory and Aging Project (n = 381) longitudinal community-based clinical-pathological studies. Dementia was based on a clinical evaluation; annual cognitive performance tests were used to create a measure of global cognition and five cognitive domains. Lewy body type was determined by using α-synuclein immunostained sections of substantia nigra, limbic and neocortical regions. Statistical models included multiple regression models for dementia and cognition and mixed effects models for decline. Cognitive fluctuations were estimated by comparing standard deviations of individual residuals from mean trajectories of decline in those with and without Lewy bodies. All models controlled for age, sex, education, Alzheimer's disease pathology and infarcts. One hundred and fifty-seven subjects (18%) exhibited Lewy body pathology (76 neocortical-type, 54 limbic-type and 27 nigra-predominant). One hundred and three (66%) subjects with Lewy body pathology had a pathologic diagnosis of Alzheimer's disease. Neocortical-type, but not nigral-predominant or limbic-type Lewy body pathology was related to an increased odds of dementia (odds ratio = 3.21; 95% confidence interval = 1.78-5.81) and lower cognition (P < 0.001) including episodic memory function (P < 0.001) proximate to death. Neocortical-type Lewy body pathology was also related to a faster decline in global cognition (P < 0.001), decline in all five specific cognitive domains (all P-values < 0.001), and to fluctuations in decline of working and semantic memory (P-values < 0.001). Limbic-type Lewy body pathology was related to lower and faster decline in visuospatial skills (P = 0.042). The relationship of Lewy body pathology to cognition and dementia was not modified by Alzheimer's disease pathology. Neocortical-type Lewy body pathology is associated with increased odds of dementia; lower and more rapid decline in all cognitive domains including episodic memory and fluctuations in decline in semantic and working memory. Limbic-type Lewy body pathology is specifically associated with lower and more rapid decline in visuospatial skills. The effect of Lewy body pathology on cognition appears to be independent of Alzheimer's disease pathology.
To assess the contribution of dementia-related neuropathologic lesions to age-related and disease-related change in cognitive function.
A total of 354 Catholic nuns, priests, and brothers had annual ...clinical evaluations for up to 13 years, died, and underwent brain autopsy. The clinical evaluations included detailed testing of cognitive function from which previously established composite measures of global cognition and specific cognitive functions were derived. As part of a uniform neuropathologic evaluation, the density of neurofibrillary tangles was summarized in a composite measure and the presence of Lewy bodies and gross and microscopic cerebral infarction was noted.
During follow-up, rate of global cognitive decline was gradual at first and then more than quadrupled in the last 4 to 5 years of life consistent with the onset of progressive dementia. Neurofibrillary tangles, cerebral infarction, and neocortical Lewy bodies all contributed to gradual age-related cognitive decline and little age-related decline was evident in the absence of these lesions. Neurofibrillary tangles and neocortical Lewy bodies contributed to precipitous disease-related cognitive decline, but substantial disease-related decline was evident even in the absence of these lesions.
Mild age-related decline in cognitive function is mainly due to the neuropathologic lesions traditionally associated with dementia.
We report the first lattice QCD calculation of the complex kaon decay amplitude A_{0} with physical kinematics, using a 32³×64 lattice volume and a single lattice spacing a, with 1/a=1.3784(68) GeV. ...We find Re(A_{0})=4.66(1.00)(1.26)×10(-7) GeV and Im(A_{0})=-1.90(1.23)(1.08)×10(-11) GeV, where the first error is statistical and the second systematic. The first value is in approximate agreement with the experimental result: Re(A_{0})=3.3201(18)×10(-7) GeV, while the second can be used to compute the direct CP-violating ratio Re(ϵ^{'}/ϵ)=1.38(5.15)(4.59)×10^{-4}, which is 2.1σ below the experimental value 16.6(2.3)×10(-4). The real part of A_{0} is CP conserving and serves as a test of our method while the result for Re(ϵ^{'}/ϵ) provides a new test of the standard model theory of CP violation, one which can be made more accurate with increasing computer capability.
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