1,802 research outputs found
The Bulge-Halo Connection in Galaxies: A Physical Interpretation of the Vcirc-sigma_0 Relation
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
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
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
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
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
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
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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Mapping The Interstellar Medium With Near-Infrared Diffuse Interstellar Bands
We map the distribution and properties of the Milky Way's interstellar medium as traced by diffuse interstellar bands (DIBs) detected in near-infrared stellar spectra from the SDSS-III/APOGEE survey. Focusing exclusively on the strongest DIB in the H band, at lambda similar to 1.527 mu m, we present a projected map of the DIB absorption field in the Galactic plane, using a set of about 60,000 sightlines that reach up to 15 kpc from the Sun and probe up to 30 mag of visual extinction. The strength of this DIB is linearly correlated with dust reddening over three orders of magnitude in both DIB equivalent width (Wpm) and extinction, with a power law index of 1.01 +/- 0.01, a mean relationship of W-DIB/A(v) = 0.1 angstrom mag(-1) and a dispersion of similar to 0.05 angstrom mag(-1) at extinctions characteristic of the Galactic midplane. These properties establish this DIB as a powerful, independent probe of dust extinction over a wide range of Av values. The subset of about 14,000 robustly detected DIB features have a W-DIB distribution that follows an exponential trend. We empirically determine the intrinsic rest wavelength of this transition to be lambda(0) = 15 272.42 angstrom and use it to calculate absolute radial velocities of the carrier, which display the kinematical signature of the rotating Galactic disk. We probe the DIB carrier distribution in three dimensions and show that it can be characterized by an exponential disk model with a scale height of about 100 pc and a scale length of about 5 kpc. Finally, we show that the DIB distribution also traces large-scale Galactic structures, including the Galactic long bar and the warp of the outer disk.NSF Astronomy & Astrophysics Postdoctoral Fellowship AST-1203017NSF AST-1109665Alfred P. Sloan FoundationNational Science FoundationU.S. Department of Energy Office of ScienceUniversity of ArizonaBrazilian Participation GroupBrookhaven National LaboratoryUniversity of CambridgeCarnegie Mellon UniversityUniversity of FloridaFrench Participation GroupGerman Participation GroupHarvard UniversityInstituto de Astrofisica de CanariasMichigan State/Notre Dame/JINA Participation GroupJohns Hopkins UniversityLawrence Berkeley National LaboratoryMax Planck Institute for AstrophysicsMax Planck Institute for Extraterrestrial PhysicsNew Mexico State UniversityNew York UniversityOhio State UniversityPennsylvania State UniversityUniversity of PortsmouthPrinceton UniversitySpanish Participation GroupUniversity of TokyoUniversity of UtahVanderbilt UniversityUniversity of VirginiaUniversity of WashingtonYale UniversitySpanish Ministry of Economy and Competitiveness AYA-2011-27754McDonald Observator
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