Welfare Regimes and “progressive” governments in Latin America: The cases of Venezuela, Ecuador and Bolivia

Several authors have applied the concept of Welfare Regimens for studying social policy in Latin America (Esping-Andersen, 1993 and 2000). Among others, Martínez Franzoni (2007) develops a typology, with fi eld work is at the turn of the millennium, and establishes three categories: State-productivist regime, state-protectionist and family orientated. Most countries in the region are placed in the latter category. The hypothesis of this article argues that with the emergence of governments considered “left” or “progressive” in several countries of the region from the late ‘90s and, more decisively, in 2000’, the map of welfare regimes models could have mutated substantively. The nationally transformative experiences are different (various socio-economic realities and political action in which they are located exists) but they have several contact points that can be summarized in a greater state intervention in different areas previously closed to their operating and recovery of important functions of welfare and care of the population by the government. The paper discusses with an exploratory and descriptive approach the welfare schemes that would shape in three countries that have constitutionalized the change from the neoliberal paradigm: Venezuela, Bolivia and Ecuador.

Familial genes in sporadic disease: Common variants of a-Synuclein gene associate with Parkinson’s disease

Genetic variation of the alpha-synuclein gene (SNCA) is known to cause familial parkinsonism, however the role of SNCA variants in sporadic Parkinson's disease (PD) remains elusive. The present study identifies an association of common SNCA polymorphisms with disease susceptibility in a series of Irish PD patients. There is evidence for association with alternate regions, of protection and risk which may act independently/synergistically, within the promoter region (Rep1; OR: 0.59, 95% CI: 0.37-0.84) and the 3'UTR of the gene (rs356165; OR: 1.67, 95% CI: 1.08-2.58). Given previous reports of association a collaborative effort is required which may exploit global linkage disequilibrium patterns for SNCA and standardise polymorphic markers used in each population. It is now crucial to identify the susceptibility allele and elucidate its functionality which may generate a therapeutic target for PD.