Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
Accumulation of the β-amyloid (Aβ) protein in cerebral blood vessels is a hallmark of Alzheimer’s disease. Soluble Aβ from the extracellular spaces of the brain is removed along the basement membranes of capillaries and basement membranes surrounding smooth muscle cells of arteries towards the surface of the brain, as intramural periarterial drainage (IPAD). This process depends on the biochemical integrity of the extracellular matrix and the strength of arterial smooth muscle cells. With ageing, possession of Apolipoprotein E4 (APOE4) genotype, hyperlipidemia, maternal high fat, immune complexes, IPAD fails, resulting in the accumulation of proteins in the walls of cerebral arteries as cerebral amyloid angiopathy. The motive force for IPAD is derived from contractions of vascular smooth muscle cells and targeting their function appears to be a promising therapeutic avenue for Alzheimer’s disease. Clusterin (Apolipoprotein J) appears to be a chaperone for Aβ, facilitating IPAD and understanding how it acts upon IPAD is a key direction in therapeutic interventions for Alzheimer’s disease.
