She was awarded a National Institute for Health Research (NIHR) lectureship at Imperial College London in 2009.[3] In 2012 she was awarded a Wellcome Trust intermediate clinical fellowship to study the misfolding of alpha-synuclein in Parkinson's disease, and how this misfolding causes neurotoxicity.[7] Gandhi established her laboratory at the UCL Queen Square Institute of Neurology in 2013.[8] Her research group develop human-derived induced pluripotent stem cell (iPSC) models of disease, with a focus on understanding how the aggregation of alpha-synuclein, a protein encoded by the SNCA gene, impacts cell physiology.[8] She makes use of single-molecule FRET and mitochondrial physiology to study the behaviour of alpha-synuclein at the molecular level.[7]
In 2016 Gandhi was awarded a secondment at the Francis Crick Institute.[9] Gandhi and co-workers showed that clumps of alpha-synuclein can be toxic to neural function, damaging proteins on the surface of mitochondria.[10][11] This damage forced a channel on mitochondria to open and made them less efficient in their production of energy, causing them to swell and leak essential chemicals – eventually causing the cell to die.[10] To perform the experiments, Gandhi and colleagues turned human skin cells into stem cells, which were converted into brain cells that could be investigated into the laboratory.[10] She was part of a team who investigated the use of exenatide as a means to slow the progression of multiple system atrophy.[12] In February 2020 Gandhi was awarded a Medical Research Council (MRC) clinical fellowship to study the fundamental origins of Parkinson's disease.[13]
During the COVID-19 pandemic, Gandhi studied the epidemiology of coronavirus disease.[14] In particular, Gandhi was interested in how the virus evolved throughout the course of the pandemic, how it impacted the nervous system and how it was transmitted between people.[14] She was also involved with the COVID-19 testing that took place at the Francis Crick Institute.[15]
Gandhi's publications[1][2] include:
- A common LRRK2 mutation in idiopathic Parkinson's disease[5]
- Mechanism of Oxidative Stress in Neurodegeneration[16]
- PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death[17]
