The Race Against Dementia Fellowship Programme will draw from the most promising scientific talent around the world; to catalyse their research work by driving a shift in culture that learns from innovation in high technology engineering research and implementation, such as in Formula 1; and to drive collaboration across disciplines and institutions to help fast-track their progress to become leaders in the field. Race Against Dementia has invested £2 million in new funding, which will be administered in partnership through Alzheimer’s Research UK, to support early-career dementia scientists. The objectives of the RAD Fellowship Scheme are:
To attract outstanding early-career scientists to the field of dementia research. To accelerate progress towards research breakthroughs through innovative and ambitious research projects. To provide these future leaders of dementia research with a unique package of flexible funding and developmental opportunities to fast-track their progress towards becoming independent research scientists. To facilitate diverse secondments that foster interdisciplinary and inter-institutional interactions on a global scale.
Lay Summary of funded fellowship Project:
In Alzheimer’s disease (AD), the loss of synapses, vital communication points between nerve cells, is thought to be the driving force behind memory loss. In AD, and related disorders such as frontotemporal dementia, tau, a normal protein found inside nerve cells, becomes “stickier”, clumping together to eventually form large aggregates called tangles. “Sticky” tau can damage synapses but evidence suggests “normal” tau is also needed to keep synapses healthy. Tau clumping may therefore be a double-edged sword; turning tau toxic whilst simultaneously preventing its normal function. Using thin slices of brain kept alive in culture dishes, we will investigate the role of normal tau in keeping synapses healthy and how this changes in AD. These slice cultures, which contain the different cell types and synapses found in an intact brain, allow us to easily test drugs and examine the sequence of changes in living tissue. This complements work in post-mortem brains, which provide a useful snapshot at the end-stages of the disease. This will help us to understand what aspects of synapse damage in AD are caused by loss of normal tau function and enable us to design and refine therapies that provide the best outcome for synapses.