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 [...]
The emerging link between O-GlcNAc and Alzheimer disease
Regional glucose hypometabolism is a defining feature of Alzheimer disease [...]
Chronic O-β-N-acetylglucosaminylase inhibition with Thiamet-G prevents tau pathology and hyperactivity in rTg4510 mice
Background: The abnormal hyperphosphorylation of the microtubule-associated protein tau plays a [...]
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 [...]
O-GlcNAc modification of tau directly inhibits its aggregation without perturbing the conformational properties of tau monomers
The aggregation of the microtubule-associated protein tau into paired helical [...]
Increasing brain protein O-GlcNAcylation mitigates breathing defects and mortality of Tau.P301L mice
The microtubule associated protein tau causes primary and secondary tauopathies [...]
Increased O-GlcNAcylation reduces pathological tau without affecting its normal phosphorylation in a mouse model of tauopathy
Neurofibrillary tangles (NFT), mainly consisting of fibrillar aggregates of hyperphosphorylated [...]
Alectos Therapeutics Announces Achievement of Preclinical Milestone in Merck Alzheimer’s Collaboration
Vancouver, British Columbia (November 16, 2012) – Alectos Therapeutics Inc. [...]
O-linked β-N-acetylglucosaminidase inhibitor attenuates β-amyloid plaque and rescues memory impairment
Deposition of β-amyloid (Aβ) as senile plaques and disrupted glucose [...]
Increasing O-GlcNAc slows neurodegeneration and stabilizes tau against aggregation
Oligomerization of tau is a key process contributing to the [...]