1,802 research outputs found

    The Bulge-Halo Connection in Galaxies: A Physical Interpretation of the Vcirc-sigma_0 Relation

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    We explore the dependence of the ratio of a galaxy's circular velocity, Vcirc, to its central velocity dispersion, sigma_0, on morphology, or equivalently total light concentration. Such a dependence is expected if light traces the mass. Over the full range of galaxy types, masses and brightnesses, and assuming that the gas velocity traces the circular velocity, we find that galaxies obey the relation log(Vcirc/sigma_0)= 0.63-0.11*C28 where C28=5log(r80/r20) and the radii are measured at 80 percent and 20 percent of the total light. Massive galaxies scatter about the Vcirc = sqrt(2)*sigma_0 line for isothermal stellar systems. Disk galaxies follow the simple relation Vcirc/sigma_0=2(1-B/T), where B/T is the bulge-to-total light ratio. For pure disks, C28~2.8, B/T -> 0, and Vcirc~=2*sigma_0. Self-consistent equilibrium galaxy models from Widrow & Dubinski (2005) constrained to match the size-luminosity and velocity-luminosity relations of disk galaxies fail to match the observed Vcirc/sigma_0 distribution. Furthermore, the matching of dynamical models for Vcirc(r)/sigma(r) with observations of dwarf and elliptical galaxies suffers from limited radial coverage and relatively large error bars; for dwarf systems, however, kinematical measurements at the galaxy center and optical edge suggest Vcirc(Rmax) > 2*sigma_0 (in contrast with past assumptions that Vcirc = sqrt(2)*sigma_0 for dwarfs.) The Vcirc-sigma_0-C28 relation has direct implications for galaxy formation and dynamical models, galaxy scaling relations, the mass function of galaxies, and the links between respective formation and evolution processes for a galaxy's central massive object, bulge, and dark matter halo.Comment: Accepted for publication in ApJL. Current version matches ApJL page requiremen

    Using the A/T/N framework to examine driving in preclinical Alzheimer’s disease

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    The A/T/N classification system is the foundation of the 2018 NIA-AA Research Framework and is intended to guide the Alzheimer disease (AD) research agenda for the next 5–10 years. Driving is a widespread functional activity that may be particularly useful in investigation of functional changes in pathological AD before onset of cognitive symptoms. We examined driving in preclinical AD using the A/T/N framework and found that the onset of driving difficulties is most associated with abnormality of both amyloid and tau pathology, rather than amyloid alone. These results have implications for participant selection into clinical trials and for the application time of interventions aimed at prolonging the time of safe driving among older adults with preclinical AD

    PDS 144: the first confirmed Herbig Ae-Herbig Ae wide binary

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    PDS 144 is a pair of Herbig Ae stars that are separated by 5.'' 35 on the sky. It has previously been shown to have an A2Ve Herbig Ae star viewed at 83 degrees inclination as its northern member and an A5Ve Herbig Ae star as its southern member. Direct imagery revealed a disk occulting PDS 144 N-the first edge-on disk observed around a Herbig Ae star. The lack of an obvious disk in direct imagery suggested PDS 144 S might be viewed face-on or not physically associated with PDS 144 N. Multi-epoch Hubble Space Telescope imagery of PDS 144 with a 5 year baseline demonstrates PDS 144 N & S are comoving and have a common proper motion with TYC 6782-878-1. TYC 6782-878-1 has previously been identified as a member of Upper Sco sub-association A at d = 145 +/- 2 pc with an age of 5-10 Myr. Ground-based imagery reveals jets and a string of Herbig-Haro knots extending 13' (possibly further) which are aligned to within 7 degrees +/- 6 degrees on the sky. By combining proper motion data and the absence of a dark mid-plane with radial velocity data, we measure the inclination of PDS 144 S to be i = 73 degrees +/- 7 degrees. The radial velocity of the jets from PDS 144 N & S indicates they, and therefore their disks, are misaligned by 25 degrees +/- 9 degrees. This degree of misalignment is similar to that seen in T Tauri wide binaries.Peer reviewe

    Loss of intranetwork and internetwork resting state functional connections with Alzheimer\u27s disease progression

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    Alzheimer\u27s disease (AD) is the most common cause of dementia. Much is known concerning AD pathophysiology but our understanding of the disease at the systems level remains incomplete. Previous AD research has used resting-state functional connectivity magnetic resonance imaging (rs-fcMRI) to assess the integrity of functional networks within the brain. Most studies have focused on the default-mode network (DMN), a primary locus of AD pathology. However, other brain regions are inevitably affected with disease progression. We studied rs-fcMRI in five functionally defined brain networks within a large cohort of human participants of either gender (n = 510) that ranged in AD severity from unaffected [clinical dementia rating (CDR) 0] to very mild (CDR 0.5) to mild (CDR 1). We observed loss of correlations within not only the DMN but other networks at CDR 0.5. Within the salience network (SAL), increases were seen between CDR 0 and CDR 0.5. However, at CDR 1, all networks, including SAL, exhibited reduced correlations. Specific networks were preferentially affected at certain CDR stages. In addition, cross-network relations were consistently lost with increasing AD severity. Our results demonstrate that AD is associated with widespread loss of both intranetwork and internetwork correlations. These results provide insight into AD pathophysiology and reinforce an integrative view of the brain\u27s functional organization

    Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism

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    Table S1. Demographic and clinical features of human subjects used in this study. Figure S1. Aβ deposition in microvessels in AD patients and APPSw/0 mice. Figure S2. Biochemical analysis of Aβ42 aggregates. Figure S3. Cy3-Aβ42 cellular uptake in wild type mouse brain slices within 30 min. Figure S4. Pericyte coverages in Lrp1lox/lox and Lrp1lox/lox; Cspg4-Cre mice. Figure S5.. LRP1 and apoE suppression with siRNA. (DOCX 1454 kb

    In vivo microdialysis reveals age-dependent decrease of brain interstitial fluid tau levels in P301S human tau transgenic mice

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    Although tau is a cytoplasmic protein, it is also found in brain extracellular fluids, e.g., CSF. Recent findings suggest that aggregated tau can be transferred between cells and extracellular tau aggregates might mediate spread of tau pathology. Despite these data, details of whether tau is normally released into the brain interstitial fluid (ISF), its concentration in ISF in relation to CSF, and whether ISF tau is influenced by its aggregation are unknown. To address these issues, we developed a microdialysis technique to analyze monomeric ISF tau levels within the hippocampus of awake, freely moving mice. We detected tau in ISF of wild-type mice, suggesting that tau is released in the absence of neurodegeneration. ISF tau was significantly higher than CSF tau and their concentrations were not significantly correlated. Using P301S human tau transgenic mice (P301S tg mice), we found that ISF tau is fivefold higher than endogenous murine tau, consistent with its elevated levels of expression. However, following the onset of tau aggregation, monomeric ISF tau decreased markedly. Biochemical analysis demonstrated that soluble tau in brain homogenates decreased along with the deposition of insoluble tau. Tau fibrils injected into the hippocampus decreased ISF tau, suggesting that extracellular tau is in equilibrium with extracellular or intracellular tau aggregates. This technique should facilitate further studies of tau secretion, spread of tau pathology, the effects of different disease states on ISF tau, and the efficacy of experimental treatments

    Regulation of beta-amyloid production in neurons by astrocyte-derived cholesterol

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    Alzheimer’s disease (AD) is characterized by the presence of amyloid β (Aβ) plaques, tau tangles, inflammation, and loss of cognitive function. Genetic variation in a cholesterol transport protein, apolipoprotein E (apoE), is the most common genetic risk factor for sporadic AD. In vitro evidence suggests that apoE links to Aβ production through nanoscale lipid compartments (lipid clusters), but its regulation in vivo is unclear. Here, we use superresolution imaging in the mouse brain to show that apoE utilizes astrocyte-derived cholesterol to specifically traffic neuronal amyloid precursor protein (APP) in and out of lipid clusters, where it interacts with β- and γ-secretases to generate Aβ-peptide. We find that the targeted deletion of astrocyte cholesterol synthesis robustly reduces amyloid and tau burden in a mouse model of AD. Treatment with cholesterol-free apoE or knockdown of cholesterol synthesis in astrocytes decreases cholesterol levels in cultured neurons and causes APP to traffic out of lipid clusters, where it interacts with α-secretase and gives rise to soluble APP-α (sAPP-α), a neuronal protective product of APP. Changes in cellular cholesterol have no effect on α-, β-, and γ-secretase trafficking, suggesting that the ratio of Aβ to sAPP-α is regulated by the trafficking of the substrate, not the enzymes. We conclude that cholesterol is kept low in neurons, which inhibits Aβ accumulation and enables the astrocyte regulation of Aβ accumulation by cholesterol signaling
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