Marta took her dementia research PHD at Bristol University, between 2011 – 2015, which was fully funded by BRACE.

Marta’s PhD project explored the relationship between two proteins, amyloid-beta (Aβ) and alpha synuclein (α-synuclein), that are found in the brains of people with dementia. These proteins have been under interest for several years due to their involvement in disease mechanisms in Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). 

A-synuclein is present in all nerve cells but becomes abnormally aggregated and forms Lewy bodies in PD, PDD and DLB. What causes the abnormal aggregation of α-synuclein is unclear, but research has indicated that a modification of α-synuclein promotes self-aggregation and nerve cell damage. In addition, Aβ play a role in the abnormal aggregation of α-synuclein. Marta used various laboratory techniques to measure specific forms of α-synuclein and Aβ in post-mortem brain samples at the South West Dementia Brain Bank. Her work demonstrated that presence of modified α-synuclein was associated with more severe disease and also strongly correlated with levels a neurotoxic form of Aβ. In addition, experiments conducted in cell culture showed a direct effect of Aβ on the modification of α-synuclein. These studies are critical in contributing to our understanding of disease mechanisms in dementia as well as aiding future potential targets for drug therapies.