Publications by authors named "E Fon"
The Canadian Consortium on Neurodegeneration in Aging (CCNA) was created by the Canadian federal government through its health research funding agency, the Canadian Institutes for Health Research (CIHR), in 2014, as a response to the G7 initiative to fight dementia. Two five-year funding cycles (2014-2019; 2019-2024) have occurred following peer review, and a third cycle (Phase 3) has just begun. A unique construct was mandated, consisting of 20 national teams in Phase I and 19 teams in Phase II (with research topics spanning from basic to clinical science to health resource systems) along with cross-cutting programs to support them.
View Article and Find Full Text PDFTarget 2035 is a global initiative that seeks to identify a pharmacological modulator of most human proteins by the year 2035. As part of an ongoing series of annual updates of this initiative, we summarise here the efforts of the EUbOPEN project whose objectives and results are making a strong contribution to the goals of Target 2035. EUbOPEN is a public-private partnership with four pillars of activity: (1) chemogenomic library collections, (2) chemical probe discovery and technology development for hit-to-lead chemistry, (3) profiling of bioactive compounds in patient-derived disease assays, and (4) collection, storage and dissemination of project-wide data and reagents.
View Article and Find Full Text PDFArticle Synopsis
- - Variants in the CTSB gene are linked to an increased risk of Parkinson's disease (PD) and affect the activity of cathepsin B, an enzyme involved in breaking down proteins and regulating cellular processes related to autophagy and lysosome function.
- - CatB can both degrade the harmful alpha-synuclein protein associated with PD and potentially create shorter versions of it that are more prone to aggregation, complicating its role in PD pathology.
- - Experiments showed that inhibiting catB disrupts autophagy and lysosomal function, leading to an accumulation of toxic protein aggregates, while activating catB enhances the clearance of these aggregates in cell and neuron models.
Article Synopsis
- Lewy bodies (LBs), which are linked to Parkinson's disease (PD), can be formed in human dopaminergic neurons derived from induced pluripotent stem cells (iPSCs) when exposed to α-synuclein fibrils and immune challenges.
- Immune response factors like interferon-γ and interleukin-1β, along with activated microglia, play a critical role in promoting this inclusion formation and impair lysosomal function.
- The study suggests that LB-like inclusions may arise from disruptions in autophagy, highlighting a possible connection between immune dysfunction and PD development.