Spatial distribution of low-energy plasma around 2 comet 67P/CG from Rosetta measurements

International audienceWe use measurements from the Rosetta plasma consortium (RPC) Langmuir probe (LAP) and mutual impedance probe (MIP) to study the spatial distribution of low-energy plasma in the near-nucleus coma of comet 67P/Churyumov-Gerasimenko. The spatial distribution is highly structured with the highest density in the summer hemisphere and above the region connecting the two main lobes of the comet, i.e. the neck region. There is a clear correlation with the neutral density and the plasma to neutral density ratio is found to be ∼1-2·10 −6 , at a cometocentric distance of 10 km and at 3.1 AU from the sun. A clear 6.2 h modulation of the plasma is seen as the neck is exposed twice per rotation. The electron density of the collisonless plasma within 260 km from the nucleus falls of with radial distance as ∼1/r. The spatial structure indicates that local ionization of neutral gas is the dominant source of low-energy plasma around the comet

Saturn’s near-equatorial ionospheric conductivities from in situ measurements

Cassini’s Grand Finale orbits provided for the first time in-situ measurements of Saturn’s topside ionosphere. We present the Pedersen and Hall conductivities of the top near-equatorial dayside ionosphere, derived from the in-situ measurements by the Cassini Radio and Wave Plasma Science Langmuir Probe, the Ion and Neutral Mass Spectrometer and the fluxgate magnetometer. The Pedersen and Hall conductivities are constrained to at least 10⁻⁵–10⁻⁴ S/m at (or close to) the ionospheric peak, a factor 10–100 higher than estimated previously. We show that this is due to the presence of dusty plasma in the near-equatorial ionosphere. We also show the conductive ionospheric region to be extensive, with thickness of 300–800 km. Furthermore, our results suggest a temporal variation (decrease) of the plasma densities, mean ion masses and consequently the conductivities from orbit 288 to 292

Effects of Peroral Omega-3 Fatty Acid Supplementation on Cerebrospinal Fluid Biomarkers in Patients with Alzheimer’s Disease: A Randomized Controlled Trial—The OmegAD Study

Background: Studies have suggested a connection between a decrease in the levels of polyunsaturated fatty acids (PUFAs) and Alzheimer’s disease (AD). We aimed to assess the effect of supplementation with omega-3 fatty acids (n-3 FAs) on biomarkers analyzed in the cerebrospinal fluid (CSF) of patients diagnosed with AD. / Objective: To investigate the effects of daily supplementation with 2.3 g of PUFAs in AD patients on the biomarkers in CSF described below. We also explored the possible correlation between these biomarkers and the performance in the cognitive test Mini-Mental State Examination (MMSE). / Methods: Thirty-three patients diagnosed with AD were randomized to either treatment with a daily intake of 2.3 g of n-3 FAs (n  =  18) or placebo (n  =  15). CSF samples were collected at baseline and after six months of treatment, and the following biomarkers were analyzed: Aβ 38, Aβ 40, Aβ 42, t-tau, p-tau, neurofilament light (NfL), chitinase-3-like protein 1 (YKL-40), acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), soluble IL-1 receptor type II (sIL-1RII), and IL-6. / Results: There were no significant differences between the groups concerning the level of the different biomarkers in the CSF at baseline. Within the treatment group, there was a small but significant increase in both YKL-40 (p = 0.04) and NfL (p = 0.03), while the other CSF biomarkers remained stable. / Conclusion: Supplementation with n-3 FAs had a statistically significant effect on NfL and YKL-40, resulting in an increase of both biomarkers, indicating a possible increase of inflammatory response and axonal damage. This increase in biomarkers did not correlate with MMSE score. / Trial registration: clinicaltrial.gov Identifier: NCT00211159

Genetic association of CDC2 with cerebrospinal fluid tau in Alzheimer's disease

We have recently reported that a polymorphism in the cell division cycle (CDC2) gene, designated Ex6 + 7I/D, is associated with Alzheimer's disease (AD). The CDC2 gene is located on chromosome 10q21.1 close to the marker D10S1225 linked to AD. Active cdc2 accumulates in neurons containing neurofibrillary tangles (NFT), a process that can precede the formation of NFT. Therefore, CDC2 is a promising candidate susceptibility gene for AD. We investigated the possible effects of the CDC2 polymorphism on cerebrospinal fluid (CSF) biomarkers in AD patients. CDC2 genotypes were evaluated in relation to CSF protein levels of total tau, phospho-tau and beta-amyloid (1-42) in AD patients and control individuals, and in relation to the amount of senile plaques and NFT in the frontal cortex and in the hippocampus in patients with autopsy-proven AD and controls. The CDC2 Ex6 + 7I allele was associated with a gene dose-dependent increase of CSF total tau levels (F-2,F- 626 = 7.0, p = 0.001) and the homozygous CDC2Ex6 +7II genotype was significantly more frequent among AD patients compared to controls (p = 0.006, OR = 1.57, 95% CI 1.13-2.17). Our results provide further evidence for an involvement of cdc2 in the pathogenesis of AD. Copyright (C) 2005 S. Karger AG, Basel

First results of electric field and density observations by Cluster EFW based on initial months of operation

International audienceHighlights are presented from studies of the electric field data from various regions along the Cluster orbit. They all point towards a very high coherence for phenomena recorded on four spacecraft that are separated by a few hundred kilometers for structures over the whole range of apparent frequencies from 1 mHz to 9 kHz. This presents completely new opportunities to study spatial-temporal plasma phenomena from the magnetosphere out to the solar wind. A new probe environment was constructed for the CLUSTER electric field experiment that now produces data of unprecedented quality. Determination of plasma flow in the solar wind is an example of the capability of the instrument

On magnetospheric electron impact ionisation and dynamics in Titan's ram-side and polar ionosphere – a Cassini case study

We present data from the sixth Cassini flyby of Titan (T5), showing that the magnetosphere of Saturn strongly interacts with the moon's ionosphere and exo-ionosphere. A simple electron ionisation model provides a reasonable agreement with the altitude structure of the ionosphere. Furthermore, we suggest that the dense and cold exo-ionosphere (from the exobase at 1430 km and outward to several Titan radii from the surface) can be explained by magnetospheric forcing and other transport processes whereas exospheric ionisation by impacting low energy electrons seems to play a minor role

Dynamical and magnetic field time constants for Titan's ionosphere: Empirical estimates and comparisons with Venus

Plasma in Titan´s ionosphere flows in response to forcing from thermal pressure gradients, magnetic forces, gravity, and ion-neutral collisions. This paper takes an empirical approach to the ionospheric dynamics by using data from Cassini instruments to estimate pressures, flow speeds, and time constants on the dayside and nightside. The plasma flow speed relative to the neutral gas speed is approximately 1 m s‑1 near an altitude of 1000 km and 200 m s‑1 at 1500 km. For comparison, the thermospheric neutral wind speed is about 100 m s‑1. The ionospheric plasma is strongly coupled to the neutrals below an altitude of about 1300 km. Transport, vertical or horizontal, becomes more important than chemistry in controlling ionospheric densities above about 1200-1500 km, depending on the ion species. Empirical estimates are used to demonstrate that the structure of the ionospheric magnetic field is determined by plasma transport (including neutral wind effects) for altitudes above about 1000 km and by magnetic diffusion at lower altitudes. The paper suggests that a velocity shear layer near 1300 km could exist at some locations and could affect the structure of the magnetic field. Both Hall and polarization electric field terms in the magnetic induction equation are shown to be locally important in controlling the structure of Titan´s ionospheric magnetic field. Comparisons are made between the ionospheric dynamics at Titan and at Venus.Fil: Cravens, T. E.. University of Kansas; Estados UnidosFil: Richard, M.. University of Kansas; Estados UnidosFil: Ma, Y. J.. University of California; Estados UnidosFil: Bertucci, Cesar. Consejo Nacional de Investigaciónes Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Astronomía y Física del Espacio. - Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Astronomía y Física del Espacio; ArgentinaFil: Luhmann, J. G.. University of California; Estados UnidosFil: Ledvina, S.. University of California; Estados UnidosFil: Robertson, I. P.. University of Kansas; Estados UnidosFil: Wahlund, J. E.. Swedish Institute of Space Physics; SueciaFil: Ågren, K.. Swedish Institute of Space Physics; SueciaFil: Cui, J.. Imperial College London; Reino UnidoFil: Muller Wodarg, I.. Imperial College London; Reino UnidoFil: Waite, J. H.. Southwest Research Institute; Estados UnidosFil: Dougherty, M.. Imperial College London; Reino UnidoFil: Bell, J.. Southwest Research Institute; Estados UnidosFil: Ulusen, D.. University of California; Estados Unido

Time‐dependent global MHD simulations of Cassini T32 flyby: From magnetosphere to magnetosheath

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95383/1/jgra19655.pd

Injury markers predict time to dementia in subjects with MCI and amyloid pathology

OBJECTIVES: Alzheimer disease (AD) can now be diagnosed in subjects with mild cognitive impairment (MCI) using biomarkers. However, little is known about the rate of decline in those subjects. In this cohort study, we aimed to assess the conversion rate to dementia and identify prognostic markers in subjects with MCI and evidence of amyloid pathology. METHODS: We pooled subjects from the VU University Medical Center Alzheimer Center and the Development of Screening Guidelines and Criteria for Predementia Alzheimer's Disease (DESCRIPA) study. We included subjects with MCI, an abnormal level of β-amyloid(1-42) (Aβ(1-42)) in the CSF, and at least one diagnostic follow-up visit. We assessed the effect of APOE genotype, CSF total tau (t-tau) and tau phosphorylated at threonine 181 (p-tau) and hippocampal volume on time to AD-type dementia using Cox proportional hazards models and on decline on the Mini-Mental State Examination (MMSE) using linear mixed models. RESULTS: We included 110 subjects with MCI with abnormal CSF Aβ(1-42) and a mean MMSE score of 26.3 ± 2.8. During a mean follow-up of 2.2 ± 1.0 (range 0.4-5.0) years, 63 subjects (57%) progressed to AD-type dementia. Abnormal CSF t-tau (hazard ratio [HR] 2.3, 95% confidence interval [CI] 1.1-4.6, p = 0.03) and CSF p-tau (HR 3.5, 95% CI 1.3-9.2, p = 0.01) concentration and hippocampal atrophy (HR 2.5, 95% CI 1.1-5.6, p = 0.02) predicted time to dementia. For subjects with both abnormal t-tau concentration and hippocampal atrophy, HR was 7.3 (95% CI 1.0-55.9, p = 0.06). Furthermore, abnormal CSF t-tau and p-tau concentrations and hippocampal atrophy predicted decline in MMSE score. CONCLUSIONS: In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline