Skyrmions in quantum Hall ferromagnets as spin-waves bound to unbalanced magnetic flux quanta

A microscopic description of (baby)skyrmions in quantum Hall ferromagnets is derived from a scattering theory of collective (neutral) spin modes by a bare quasiparticle. We start by mapping the low lying spectrum of spin waves in the uniform ferromagnet onto that of free moving spin excitons, and then we study their scattering by the defect of charge. In the presence of this disturbance, the local spin stiffness varies in space, and we translate it into an inhomogeneus metric in the Hilbert space supporting the excitons. An attractive potencial is then required to preserve the symmetry under global spin rotations, and it traps the excitons around the charged defect. The quasiparticle now carries a spin texture. Textures containing more than one exciton are described within a mean-field theory, the interaction among the excitons being taken into account through a new renormalization of the metric. The number of excitons actually bound depends on the Zeeman coupling, that plays the same role as a chemical potencial. For small Zeeman energies, the defect binds many excitons which condensate. As the bound excitons have a unit of angular momentum, provided by the quantum of magnetic flux left unbalanced by the defect of charge, the resulting texture turns out to be a topological excitation of charge 1. Its energy is that given by the non-linear sigma model for the ground state in this topological sector, i.e. the texture is a skyrmion.Comment: 17 pages, 1 figur

The Role of Presenilin and its Interacting Proteins in the Biogenesis of Alzheimer’s Beta Amyloid

The biogenesis and accumulation of the beta amyloid protein (Aβ) is a key event in the cascade of oxidative and inflammatory processes that characterises Alzheimer’s disease. The presenilins and its interacting proteins play a pivotal role in the generation of Aβ from the amyloid precursor protein (APP). In particular, three proteins (nicastrin, aph-1 and pen-2) interact with presenilins to form a large multi-subunit enzymatic complex (γ-secretase) that cleaves APP to generate Aβ. Reconstitution studies in yeast and insect cells have provided strong evidence that these four proteins are the major components of the γ-secretase enzyme. Current research is directed at elucidating the roles that each of these protein play in the function of this enzyme. In addition, a number of presenilin interacting proteins that are not components of γ-secretase play important roles in modulating Aβ production. This review will discuss the components of the γ-secretase complex and the role of presenilin interacting proteins on γ-secretase activity

Increased expression of receptor phosphotyrosine phosphatase-β/ζ is associated with molecular, cellular, behavioral and cognitive schizophrenia phenotypes

Schizophrenia is a serious and chronic mental disorder, in which both genetic and environmental factors have a role in the development of the disease. Neuregulin-1 (NRG1) is one of the most established genetic risk factors for schizophrenia, and disruption of NRG1 signaling has been reported in this disorder. We reported previously that NRG1/ErbB4 signaling is inhibited by receptor phosphotyrosine phosphatase-β/ζ (RPTP β/ζ) and that the gene encoding RPTPβ/ζ (PTPRZ1) is genetically associated with schizophrenia. In this study, we examined the expression of RPTPβ/ζ in the brains of patients with schizophrenia and observed increased expression of this gene. We developed mice overexpressing RPTPβ/ζ (PTPRZ1-transgenic mice), which showed reduced NRG1 signaling, and molecular and cellular changes implicated in the pathogenesis of schizophrenia, including altered glutamatergic, GABAergic and dopaminergic activity, as well as delayed oligodendrocyte development. Behavioral analyses also demonstrated schizophrenia-like changes in the PTPRZ1-transgenic mice, including reduced sensory motor gating, hyperactivity and working memory deficits. Our results indicate that enhanced RPTPβ/ζ signaling can contribute to schizophrenia phenotypes, and support both construct and face validity for PTPRZ1-transgenic mice as a model for multiple schizophrenia phenotypes. Furthermore, our results implicate RPTPβ/ζ as a therapeutic target in schizophrenia