The themes of the 1st day of the main AD conference were Frontotemporal dementia, Neurovascular dysfunction, and Inflammation & Immunity. One of many fascinating presentations on this was given by Jessica Duncombe, a 3rd year PhD student from the University of Edinburgh. Jessica Duncombe hypothesised that dysfunctions in neurovascular coupling may underlie changes in AD and normal ageing. The researchers looked at TgSwDI transgenic mice and their wild type littermates, focusing on the cortex. Interestingly, both wild type and transgenic mice showed an impaired vascular response to whisker stimulation as well as increased microglial proliferation. Whilst no difference in vascular response was seen between wild-type and transgenic mice, microglial proliferation was enhanced in the transgenic mice, who also showed significantly more amyloid at 24 months (although not 6 months).
Professor Rusted presented a poster on day 1 of the conference, as shown below.
The themes of the 2nd day of the main conference were Models of Neurodegeneration, New Treatments for Dementia, Mechanisms of Cell Death and Tau, and AB: Two Sides of the Same Coin? Sadly, one scheduled presenter was unable to make the conference, but Dr Jack Rivers-Auty from the University of Manchester was able to step in with an interesting talk on zinc deficiency, neuroinflammation, and AD. Dr Rivers-Auty had a very engaging presentation style and set of slides; he started the talk with a countdown timer, showing the difference in rate of neuron loss in a healthy brain, and an AD brain, with an associated image of progressive atrophy – a very effective demonstration. Dr Rivers-Auty looked at IL-1b, a potential molecular mediator of the inflammatory response, the production of which is regulated by inflammasomes including NLRP3. Zinc absorption reduces in ageing, with AD patients presenting with lower plasma and serum zinc levels. Dr River-Auty hypothesised that zinc deficiency causes NLRP3 sensitivity, resulting in neuroinflammation and exacerbating AD. Evidence for this comes from APP-PS1 zinc deficient (AD zd), APP-PS1 zinc normal (AD zn), wild type zinc deficient (WT zd) and wild type zinc normal mice (WT zn). AD zinc deficient mice showed poorer Y-maze performance and a lack of morris water maze improvement (between 3-6 months) when compared with AD zn, WT zd and WT zn mice. It appears that zinc deficiency resulted in earlier impairments in the AD mice alone, therefore seemingly exacerbating the AD phenotype.
A particularly interesting poster was presented by Dr Chris Henstridge from the University of Edinburgh, reporting on the first post mortem analysis of a brain from the Lothian 1936 birth cohort. Having spoken with Dr Henstridge, it seems they now have four donated brains. As this cohort had APOE status and cognitive testing from 7 years old onwards, these upcoming post mortem analyses could be of interest.
Whilst the conference content overall was quite molecular, it was still very good to know what is going on in the general area of AD research. I found the conference useful for improving the way in which I communicate my research to others, and for taking note of particularly effective presenting styles (through both posters and talks). Moreover, it was very helpful in deepening my level of understanding of the type of research the other PhD students in the AD Society DTC will be undertaking, especially as one conference theme centred on drug discovery (related to Lucas Kraft’s research).