Individual- and area-level socioeconomic inequalities in diabetes mellitus in Saskatchewan between 2007 and 2012: a cross-sectional analysis.

Background: Improving our understanding of social inequalities may improve prevention and treatment efforts for diabetes mellitus. We examined the association between individual- and area-level socioeconomic measures and physician-diagnosed diabetes in Saskatchewan over time.

Methods: In this cross-sectional study, we linked health administrative data with individual-level socioeconomic data from the Canadian Community Health Survey and area-level data from the 2006 Canadian census.

α-Synuclein increases β-amyloid secretion by promoting β-/γ-secretase processing of APP.

α-Synuclein misfolding and aggregation is often accompanied by β-amyloid deposition in some neurodegenerative diseases. We hypothesised that α-synuclein promotes β-amyloid production from APP. β-Amyloid levels and APP amyloidogenic processing were investigated in neuronal cell lines stably overexpressing wildtype and mutant α-synuclein.

Seeking a mechanism for the toxicity of oligomeric α-synuclein.

In a number of neurological diseases including Parkinson's disease (PD), α-synuclein is aberrantly folded, forming abnormal oligomers, and amyloid fibrils within nerve cells. Strong evidence exists for the toxicity of increased production and aggregation of α-synuclein in vivo. The toxicity of α-synuclein is popularly attributed to the formation of "toxic oligomers": a heterogenous and poorly characterized group of conformers that may share common molecular features.