Detecting Neutrino Magnetic Moments with Conducting Loops

It is well established that neutrinos have mass, yet it is very difficult to measure those masses directly. Within the standard model of particle physics, neutrinos will have an intrinsic magnetic moment proportional to their mass. We examine the possibility of detecting the magnetic moment using a conducting loop. According to Faraday's Law of Induction, a magnetic dipole passing through a conducting loop induces an electromotive force, or EMF, in the loop. We compute this EMF for neutrinos in several cases, based on a fully covariant formulation of the problem. We discuss prospects for a real experiment, as well as the possibility to test the relativistic formulation of intrinsic magnetic moments.Comment: 6 pages, 4 b/w figures, uses RevTe

Random projections and the optimization of an algorithm for phase retrieval

Iterative phase retrieval algorithms typically employ projections onto constraint subspaces to recover the unknown phases in the Fourier transform of an image, or, in the case of x-ray crystallography, the electron density of a molecule. For a general class of algorithms, where the basic iteration is specified by the difference map, solutions are associated with fixed points of the map, the attractive character of which determines the effectiveness of the algorithm. The behavior of the difference map near fixed points is controlled by the relative orientation of the tangent spaces of the two constraint subspaces employed by the map. Since the dimensionalities involved are always large in practical applications, it is appropriate to use random matrix theory ideas to analyze the average-case convergence at fixed points. Optimal values of the gamma parameters of the difference map are found which differ somewhat from the values previously obtained on the assumption of orthogonal tangent spaces.Comment: 15 page

Phasing diffuse scattering. Application of the SIR2002 algorithm to the non-crystallographic phase problem

A new phasing algorithm has been used to determine the phases of diffuse elastic X-ray scattering from a non-periodic array of gold balls of 50 nm diameter. Two-dimensional real-space images, showing the charge-density distribution of the balls, have been reconstructed at 50 nm resolution from transmission diffraction patterns recorded at 550 eV energy. The reconstructed image fits well with scanning electron microscope (SEM) image of the same sample. The algorithm, which uses only the density modification portion of the SIR2002 program, is compared with the results obtained via the Gerchberg-Saxton-Fienup HIO algorithm. In this way the relationship between density modification in crystallography and the HiO algorithm used in signal and image processing is elucidated.Comment: 7 pages, 12 figure

Analytical evaluation of atomic form factors: application to Rayleigh scattering

Atomic form factors are widely used for the characterization of targets and specimens, from crystallography to biology. By using recent mathematical results, here we derive an analytical expression for the atomic form factor within the independent particle model constructed from nonrelativistic screened hydrogenic wavefunctions. The range of validity of this analytical expression is checked by comparing the analytically obtained form factors with the ones obtained within the Hartee-Fock method. As an example, we apply our analytical expression for the atomic form factor to evaluate the differential cross section for Rayleigh scattering off neutral atoms.Comment: 7 pages, 1 figur

Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease

Alterations of the dopaminergic (DAergic) system are frequently reported in Alzheimer’s disease (AD) patients and are commonly linked to cognitive and non-cognitive symptoms. However, the cause of DAergic system dysfunction in AD remains to be elucidated. We investigated alterations of the midbrain DAergic system in the Tg2576 mouse model of AD, overexpressing a mutated human amyloid precursor protein (APPswe). Here, we found an age-dependent DAergic neuron loss in the ventral tegmental area (VTA) at pre-plaque stages, although substantia nigra pars compacta (SNpc) DAergic neurons were intact. The selective VTA DAergic neuron degeneration results in lower DA outflow in the hippocampus and nucleus accumbens (NAc) shell. The progression of DAergic cell death correlates with impairments in CA1 synaptic plasticity, memory performance and food reward processing. We conclude that in this mouse model of AD, degeneration of VTA DAergic neurons at pre-plaque stages contributes to memory deficits and dysfunction of reward processing

Third structure determination by powder diffractometry round robin (SDPDRR-3)

The results from a third structure determination by powder diffractometry (SDPD) round robin are discussed. From the 175 potential participants having downloaded the powder data, nine sent a total of 12 solutions (8 and 4 for samples 1 and 2, respectively, a tetrahydrated calcium tartrate and a lanthanum tungstate). Participants used seven different computer programs for structure solution (ESPOIR, EXPO, FOX, PSSP, SHELXS, SUPERFLIP, and TOPAS), applying Patterson, direct methods, direct space methods, and charge flipping approach. It is concluded that solving a structure from powder data remains a challenge, at least one order of magnitude more difficult than solving a problem with similar complexity from single-crystal data. Nevertheless, a few more steps in the direction of increasing the SDPD rate of success were accomplished since the two previous round robins: this time, not only the computer program developers were successful but also some users. No result was obtained from crystal structure prediction expert

Systemic delivery of a specific antibody targeting the pathological N-terminal truncated tau peptide reduces retinal degeneration in a mouse model of Alzheimer’s Disease

Retina and optic nerve are sites of extra-cerebral manifestations of Alzheimer’s Disease (AD). Amyloid-β (Aβ) plaques and neurofibrillary tangles of hyperphosphorylated tau protein are detected in eyes from AD patients and transgenic animals in correlation with inflammation, reduction of synapses, visual deficits, loss of retinal cells and nerve fiber. However, neither the pathological relevance of other post-translational tau modifications—such as truncation with generation of toxic fragments—nor the potential neuroprotective action induced by their in vivo clearance have been investigated in the context of AD retinal degeneration. We have recently developed a monoclonal tau antibody (12A12mAb) which selectively targets the neurotoxic 20–22 kDa NH2-derived peptide generated from pathological truncation at the N-terminal domain of tau without cross-reacting with its full-length normal protein. Previous studies have shown that 12A12mAb, when intravenously (i.v.)-injected into 6-month-old Tg2576 animals, markedly improves their AD-like, behavioural and neuropathological syndrome. By taking advantage of this well-established tau-directed immunization regimen, we found that 12A12mAb administration also exerts a beneficial action on biochemical, morphological and metabolic parameters (i.e. APP/Aβ processing, tau hyperphosphorylation, neuroinflammation, synaptic proteins, microtubule stability, mitochondria-based energy production, neuronal death) associated with ocular injury in the AD phenotype. These findings prospect translational implications in the AD field by: (1) showing for the first time that cleavage of tau takes part in several pathological changes occurring in vivo in affected retinas and vitreous bodies and that its deleterious effects are successfully antagonized by administration of the specific 12A12mAb; (2) shedding further insights on the tight connections between neurosensory retina and brain, in particular following tau-based immunotherapy. In our view, the parallel response we detected in this preclinical animal model, both in the eye and in the hippocampus, following i.v. 12A12mAb injection opens novel diagnostic and therapeutic avenues for the clinical management of cerebral and extracerebral AD signs in human beings

Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease

Alterations of the dopaminergic (DAergic) system are frequently reported in Alzheimer's disease (AD) patients and are commonly linked to cognitive and non-cognitive symptoms. However, the cause of DAergic system dysfunction in AD remains to be elucidated. We investigated alterations of the midbrain DAergic system in the Tg2576 mouse model of AD, overexpressing a mutated human amyloid precursor protein (APPswe). Here, we found an age-dependent DAergic neuron loss in the ventral tegmental area (VTA) at pre-plaque stages, although substantia nigra pars compacta (SNpc) DAergic neurons were intact. The selective VTA DAergic neuron degeneration results in lower DA outflow in the hippocampus and nucleus accumbens (NAc) shell. The progression of DAergic cell death correlates with impairments in CA1 synaptic plasticity, memory performance and food reward processing. We conclude that in this mouse model of AD, degeneration of VTA DAergic neurons at pre-plaque stages contributes to memory deficits and dysfunction of reward processing

Passive immunotherapy for N-truncated tau ameliorates the cognitive deficits in two mouse AD models

Clinical and neuropathological studies have shown that tau pathology better correlates with the severity of dementia than amyloid plaque burden, making tau an attractive target for the cure of Alzheimer\u2019s disease. We have explored whether passive immunization with the 12A12 monoclonal antibody (26\u201336aa of tau protein) could improve the Alzheimer\u2019s disease phenotype of two well-established mouse models, Tg2576 and 3xTg mice. 12A12 is a cleavage-specific monoclonal antibody which selectively binds the pathologically relevant neurotoxic NH226-230 fragment (i.e. NH2htau) of tau protein without cross-reacting with its full-length physiological form(s). We found out that intravenous administration of 12A12 monoclonal antibody into symptomatic (6 months old) animals: (i) reaches the hippocampus in its biologically active (antigen-binding competent) form and successfully neutralizes its target; (ii) reduces both pathological tau and amyloid precursor protein/amyloid\u3b2 metabolisms involved in early disease-associated synaptic deterioration; (iii) improves episodic-like type of learning/memory skills in hippocampal-based novel object recognition and object place recognition behavioural tasks; (iv) restores the specific up-regulation of the activity-regulated cytoskeleton-associated protein involved in consolidation of experience-dependent synaptic plasticity; (v) relieves the loss of dendritic spine connectivity in pyramidal hippocampal CA1 neurons; (vi) rescues the Alzheimer\u2019s disease-related electrophysiological deficits in hippocampal long-term potentiation at the CA3-CA1 synapses; and (vii) mitigates the neuroinflammatory response (reactive gliosis). These findings indicate that the 20\u201322 kDa NH2-terminal tau fragment is crucial target for Alzheimer\u2019s disease therapy and prospect immunotherapy with 12A12 monoclonal antibody as safe (normal tau-preserving), beneficial approach in contrasting the early Amyloid\u3b2-dependent and independent neuropathological and cognitive alterations in affected subject