Latest Publications
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 [...]
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 [...]
Alectos Therapeutics Announces Achievement of Phase I Clinical Milestone in Merck Alzheimer’s Collaboration
Vancouver, British Columbia (December 12, 2014) – Alectos Therapeutics Inc. today announced the initiation of a Phase I clinical trial in its collaboration with Merck, known as MSD outside the U.S. and Canada, to identify [...]
Alectos Announces Preclinical Results in TAPP Mouse Model of Alzheimer’s Disease
Oct 26, 2014 – Alectos today announced publication of preclinical studies showing that pharmacological inhibition of O-GlcNAcase (OGA) prevents cognitive decline and amyloid plaque formation in the TAPP mouse model of Alzheimer’s disease. For details, [...]
Pharmacological inhibition of O-GlcNAcase (OGA) prevents cognitive decline and amyloid plaque formation in bigenic tau/APP mutant mice
BACKGROUND: Amyloid plaques and neurofibrillary tangles (NFTs) are the defining pathological hallmarks of Alzheimer's disease (AD). Increasing the quantity of the O-linked N-acetylglucosamine (O-GlcNAc) post-translational modification of nuclear and cytoplasmic proteins slows neurodegeneration and blocks [...]
The emerging link between O-GlcNAc and Alzheimer disease
Regional glucose hypometabolism is a defining feature of Alzheimer disease (AD). One emerging link between glucose hypometabolism and progression of AD is the nutrient-responsive post-translational O-GlcNAcylation of nucleocytoplasmic proteins. O-GlcNAc is abundant in neurons and [...]