Race Against Dementia Fellow
University College London, UK
Dr Croft aims to understand how known risk genes link to the development of signature disease pathologies and neurodegeneration in dementia, and whether these processes can be targeted by new treatments. She was awarded the Race Against Dementia Fellowship in 2019.
Cara completed an undergraduate master’s degree in neuroscience at the University of Manchester, before embarking on an NC3Rs-funded Neuroscience PhD studentship at King’s College London, UK.
Prior to taking up the RAD Fellowship, Cara worked as a postdoctoral research associate at the University of Florida.
“Dementia knows no borders and our research shouldn’t either. The RAD network enables international collaborations so I can work alongside some of the best researchers in the world. I truly feel we will only make steps in dementia research if we are working together globally.”
Dr Cara Croft
Research summary
Alzheimer’s disease and Parkinson’s disease are some of the most common causes of dementia leading to loss of memory, thoughts, motor skills and other symptoms which affect day to day living. It is also known that a build-up of certain proteins in brain cells are closely linked to these symptoms and the overall health of brain cells. Tau protein build-up is heavily implicated in Alzheimer’s disease as well as frontotemporal dementia. Whereas the synuclein protein builds-up in Parkinson’s disease and dementia with Lewy bodies.
Research has also identified many changes in the genetic code which are associated with the development of the diseases that cause dementia. Many of these genetic changes have been found but have not been studied in depth and may lead to new dementia treatments.
Dr Croft’s Race Against Dementia Fellowship aims to understand how some of these genetic changes affect this protein build-up and brain cell health. She will develop new technologies to help understand how these genes affect protein build-up and brain cell health and function. Using these new technologies with brain in a petri dish models and animal models with features of disease should help uncover whether new therapies should target these changes in the genetic code or protein build up.
