Statistics of Neutron Stars at the Stage of Supersonic Propeller

We analyze the statistical distribution of neutron stars at the stage of a supersonic propeller. An important point of our analysis is allowance for the evolution of the angle of inclination of the magnetic axis to the spin axis of the neutron star for the boundary of the transition to the supersonic propeller stage for two models: the model with hindered particle escape from the stellar surface and the model with free particle escape. As a result, we have shown that a consistent allowance for the evolution of the inclination angle in the region of extinct radio pulsars for the two models leads to an increase in the total number of neutron stars at the supersonic propeller stage. This increase stems from he fact that when allowing for the evolution of the inclination angle $\chi$ for neutron stars in the region of extinct radio pulsars and, hence, for the boundary of the transition to the propeller stage, this transition is possible at shorter spin periods (P~5-10 s) than assumed in the standard model.Comment: 15 pages, 6 figures; scale corrected for figures 3-

Cosmology and Neutrino Properties

This is a brief review for particle physicists on cosmological impact of neutrinos and on restrictions on neutrino properties from cosmology. The paper includes discussion of upper bounds on neutrino mass and possible ways to relax them, methods to observe the cosmic neutrino background, bounds on the cosmological lepton asymmetry which are strongly improved by neutrino oscillations, cosmological effects of breaking of spin-statistics theorem for neutrinos, bounds on mixing parameters of active and possible sterile neutrinos with the account of active neutrino oscillations, bounds on right-handed currents and neutrino magnetic moments, and some more.Comment: Talk presented at the meeting of Nuclear Physics Division of Russian Academy of Sci., November, 2007, Moscow. 21 pages, 3 figures. One reference is added and some numbers are slightly correcte

Alzheimer disease models and human neuropathology: similarities and differences

Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease. Numerous mouse transgenic lines have now succeeded in partially reproducing its lesions: the extracellular deposits of Aβ peptide and the intracellular accumulation of tau protein. Mutated human APP transgenes result in the deposition of Aβ peptide, similar but not identical to the Aβ peptide of human senile plaque. Amyloid angiopathy is common. Besides the deposition of Aβ, axon dystrophy and alteration of dendrites have been observed. All of the mutations cause an increase in Aβ 42 levels, except for the Arctic mutation, which alters the Aβ sequence itself. Overexpressing wild-type APP alone (as in the murine models of human trisomy 21) causes no Aβ deposition in most mouse lines. Doubly (APP × mutated PS1) transgenic mice develop the lesions earlier. Transgenic mice in which BACE1 has been knocked out or overexpressed have been produced, as well as lines with altered expression of neprilysin, the main degrading enzyme of Aβ. The APP transgenic mice have raised new questions concerning the mechanisms of neuronal loss, the accumulation of Aβ in the cell body of the neurons, inflammation and gliosis, and the dendritic alterations. They have allowed some insight to be gained into the kinetics of the changes. The connection between the symptoms, the lesions and the increase in Aβ oligomers has been found to be difficult to unravel. Neurofibrillary tangles are only found in mouse lines that overexpress mutated tau or human tau on a murine tau −/− background. A triply transgenic model (mutated APP, PS1 and tau) recapitulates the alterations seen in AD but its physiological relevance may be discussed. A number of modulators of Aβ or of tau accumulation have been tested. A transgenic model may be analyzed at three levels at least (symptoms, lesions, cause of the disease), and a reading key is proposed to summarize this analysis