Focal Point Gallery : a new institutional model?

A description is given of how Focal Point Gallery’s (FPG) new building (in Southend-on-Sea, Essex) was conceived in terms of its practical effectiveness in addressing tensions between local and global, utopian, social and political thought, through the commissioning of permanent and temporary artworks – by Marc Camille Chaimowicz, Scott King, Mike Nelson, Elizabeth Price, Allen Rupperberg, Tris Vonna-Michell and Lawrence Weiner – via an ethical curatorial approach involving affirmative modes of criticality. This includes an account of distribution strategies used for FPG’s printed publicity as an artistic program in its own right, and the various platforms, channels and spaces of editorial circulation that informed this curatorial approach

Modes of Aβ toxicity in Alzheimer’s disease

Alzheimer’s disease (AD) is reaching epidemic proportions, yet a cure is not yet available. While the genetic causes of the rare familial inherited forms of AD are understood, the causes of the sporadic forms of the disease are not. Histopathologically, these two forms of AD are indistinguishable: they are characterized by amyloid-β (Aβ) peptide-containing amyloid plaques and tau-containing neurofibrillary tangles. In this review we compare AD to frontotemporal dementia (FTD), a subset of which is characterized by tau deposition in the absence of overt plaques. A host of transgenic animal AD models have been established through the expression of human proteins with pathogenic mutations previously identified in familial AD and FTD. Determining how these mutant proteins cause disease in vivo should contribute to an understanding of the causes of the more frequent sporadic forms. We discuss the insight transgenic animal models have provided into Aβ and tau toxicity, also with regards to mitochondrial function and the crucial role tau plays in mediating Aβ toxicity. We also discuss the role of miRNAs in mediating the toxic effects of the Aβ peptide

Full-genome scan for linkage in 50 families segregating the bipolar affective disease phenotype

A genome scan of similar to 12-cM initial resolution was done on 50 of a set of 51 carefully ascertained unilineal multiplex families segregating the bipolar affective disorder phenotype. In addition to standard multipoint linkage analysis methods, a simultaneous-search algorithm was applied in an attempt to surmount the problem of genetic heterogeneity. The results revealed no linkage across the genome. The results exclude monogenic models and make it unlikely that two genes account for the disease in this sample. These results support the conclusion that at least several hundred kindreds will be required in order to establish linkage of susceptibility loci to bipolar disorder in heterogeneous populations