Alectos Supports NSERC Funding for Prof. A.J. Bennet at SFU

Feb 11, 2016 – Alectos today announced its support for NSERC funding for the group of Prof. A.J. Bennet at Simon Fraser University, Department of Chemistry, in a project titled “Fundamental Studies on the Biochemical Mechanism of Chemical Chaperoning of Glucocerebrosidase”. Parkinson's disease is a worldwide health problem that has been linked to deficiencies in [...]

February 11th, 2016|Tags: , , , , |

O-GlcNAc modification blocks the aggregation and toxicity of the protein α-synuclein associated with Parkinson’s disease

Several aggregation-prone proteins associated with neurodegenerative diseases can be modified by O-linked N-acetyl-glucosamine (O-GlcNAc) in vivo. One of these proteins, α-synuclein, is a toxic aggregating protein associated with synucleinopathies, including Parkinson's disease. However, the effect of O-GlcNAcylation on α-synuclein is not clear. Here, we use synthetic protein chemistry to generate both unmodified α-synuclein and α-synuclein [...]

October 12th, 2015|Tags: , , |

Fluorescence-quenched substrates for live cell imaging of human glucocerebrosidase activity

Deficiency of the lysosomal glycoside hydrolase glucocerebrosidase (GCase) leads to abnormal accumulation of glucosyl ceramide in lysosomes and the development of the lysosomal storage disease known as Gaucher's disease. More recently, mutations in the GBA1 gene that encodes GCase have been uncovered as a major genetic risk factor for Parkinson's disease (PD). Current therapeutic strategies [...]

January 15th, 2015|Tags: , , |

Alectos Supports NSERC Funding for Prof. M.J. Boulanger at UVic

Oct 6, 2014 – Alectos today announced its support for NSERC funding for the group of Prof. M.J. Boulanger at the University of Victoria, Department of Biochemistry & Microbiology, in a project titled “Cloning and expression of human glucocerebrosidase”. Parkinson’s disease (PD) is a worldwide health problem that is characterized by the buildup of abnormal [...]

October 6th, 2014|Tags: , , , , |

O-GlcNAc and neurodegeneration: biochemical mechanisms and potential roles in Alzheimer’s disease and beyond

Alzheimer disease (AD) is a growing problem for aging populations worldwide. Despite significant efforts, no therapeutics are available that stop or slow progression of AD, which has driven interest in the basic causes of AD and the search for new therapeutic strategies. Longitudinal studies have clarified that defects in glucose metabolism occur in patients exhibiting [...]

April 24th, 2014|Tags: , , , , , , , , |

O-GlcNAc modification prevents peptide-dependent acceleration of α-synuclein aggregation

Sweet relief: the Parkinson's disease-associated protein α-synuclein is post-translationally modified by N-acetylglucosamine (O-GlcNAc), but the biochemical consequences are unknown. Here we show that an O-GlcNAc-modified peptide does not participate in α-synuclein aggregation, thus suggesting that O-GlcNAc might directly inhibit aggregation in cells. Source: Marotta, N.P. et al. Chembiochem 13(18), 2665-2670 (2012).

November 9th, 2012|Tags: , , |