Leave it to the Amateurs: A Career Development Explanation of Political Inexperience among Members of the Canadian Parliament:MA Thesis

In many advanced democracies, political scientists have lamented the rise of professional politicians as a challenge to the effective representation of diverse electorates. In contrast, their relative absence from Canadian federal politics gives rise to concerns over high levels of political amateurism among Canadian MPs. This study, thus, seeks to account for the numerical weakness of individuals with an occupational background in politics in the Canadian Parliament. It utilizes both individual-level quantitative data on MPs serving between the 35th and 41st Parliaments, inclusive, as well as material from qualitative interviews with over seventy former MPs. Conceptualizing the field of politics as a career in itself, and drawing on career development theory, the study finds that at the key stages of establishing, maintaining, and disengaging from a federal political career, there are specific challenges that are not significantly ameliorated by the possession of professional experience in politics itself. Professional politicians, therefore, have no major advantage over those with non-political occupational backgrounds in their career development. Furthermore, by acknowledging the existence of different types of professional politician, it finds that those whose primary occupational background was in politics itself to be in a distinct minority, but the extent of political amateurism is challenged by a much larger minority of MPs whose primary occupation was non-political but who still possess some secondary or electoral experience prior to entering Parliament.

Rare coding variants in the phospholipase D3 gene confer risk for Alzheimer's disease.

Genome-wide association studies (GWAS) have identified several risk variants for late-onset Alzheimer's disease (LOAD)1, 2. These common variants have replicable but small effects on LOAD risk and generally do not have obvious functional effects. Low-frequency coding variants, not detected by GWAS, are predicted to include functional variants with larger effects on risk. To identify low-frequency coding variants with large effects on LOAD risk, we carried out whole-exome sequencing (WES) in 14 large LOAD families and follow-up analyses of the candidate variants in several large LOAD case–control data sets. A rare variant in PLD3 (phospholipase D3; Val232Met) segregated with disease status in two independent families and doubled risk for Alzheimer’s disease in seven independent case–control series with a total of more than 11,000 cases and controls of European descent. Gene-based burden analyses in 4,387 cases and controls of European descent and 302 African American cases and controls, with complete sequence data for PLD3, reveal that several variants in this gene increase risk for Alzheimer’s disease in both populations. PLD3 is highly expressed in brain regions that are vulnerable to Alzheimer’s disease pathology, including hippocampus and cortex, and is expressed at significantly lower levels in neurons from Alzheimer’s disease brains compared to control brains. Overexpression of PLD3 leads to a significant decrease in intracellular amyloid-β precursor protein (APP) and extracellular Aβ42 and Aβ40 (the 42- and 40-residue isoforms of the amyloid-β peptide), and knockdown of PLD3 leads to a significant increase in extracellular Aβ42 and Aβ40. Together, our genetic and functional data indicate that carriers of PLD3 coding variants have a twofold increased risk for LOAD and that PLD3 influences APP processing. This study provides an example of how densely affected families may help to identify rare variants with large effects on risk for disease or other complex traits.