All Outputs (4)

Breaking the Cycle, Cholesterol Cycling, and Synapse Damage in Response to Amyloid-ß (2017)
Journal Article
Bate, C. (2017). Breaking the Cycle, Cholesterol Cycling, and Synapse Damage in Response to Amyloid-ß. Journal of Experimental Neuroscience, 11, https://doi.org/10.1177/1179069517733096

Soluble amyloid-β (Aβ) oligomers, a key driver of pathogenesis in Alzheimer disease, bind to cellular prion proteins (PrPC) expressed on synaptosomes resulting in increased cholesterol concentrations, movement of cytoplasmic phospholipase A2 (cPLA2)... Read More about Breaking the Cycle, Cholesterol Cycling, and Synapse Damage in Response to Amyloid-ß.

Can we switch production of toxic Aß oligomers to neuroprotective Aß monomers to allow synapse regeneration? (2017)
Journal Article
Bate, C. (2017). Can we switch production of toxic Aß oligomers to neuroprotective Aß monomers to allow synapse regeneration?. Neural Regeneration Research, 12(9), 1437-1438. https://doi.org/10.4103/1673-5374.215252

The cholesterol ester cycle regulates signalling complexes and synapse damage caused by amyloid-ß (2017)
Journal Article
West, E., Osborne, C., & Bate, C. (2017). The cholesterol ester cycle regulates signalling complexes and synapse damage caused by amyloid-ß. Journal of Cell Science, 130, 3050-3059. https://doi.org/10.1242/jcs.205484

Cholesterol is required for the formation and function of some signalling platforms. In synaptosomes, amyloid-β (Aβ) oligomers, the causative agent in Alzheimer's disease, bind to cellular prion proteins (PrPC) resulting in increased cholesterol conc... Read More about The cholesterol ester cycle regulates signalling complexes and synapse damage caused by amyloid-ß.

Sialylated glycosylphosphatidylinositols suppress the production of toxic amyloid-ß oligomers (2017)
Journal Article
Nolan, W., McHale-Owen, H., & Bate, C. (2017). Sialylated glycosylphosphatidylinositols suppress the production of toxic amyloid-ß oligomers. Biochemical Journal, 474(17), 3045-3058. https://doi.org/10.1042/BCJ20170239

The production of amyloid-β (Aβ) is a key factor driving pathogenesis in Alzheimer's disease (AD). Increasing concentrations of soluble Aβ oligomers within the brain lead to synapse degeneration and the progressive dementia characteristic of AD. Sinc... Read More about Sialylated glycosylphosphatidylinositols suppress the production of toxic amyloid-ß oligomers.