Keywords
Clinical Conditions
Equipment & Techniques
I am a Post-Doctoral Research Associate in the Williams-Gray/Barker lab at the John Van Geest Centre for Brain Repair. This work focusses on detecting and treating Parkinson’s Disease (PD) and the associated dementia (PDD) earlier across a few different studies. NET-PDD is an ongoing longitudinal study focussing on the progression of PD, the development of PDD, the PET imaging hallmarks via Tau ([18F]AV1451) as well as neuroinflammation via microglial activation ([11C]PK11195), the MRI-detected neuroanatomical signatures, the related blood/CSF cytokines, and the related bio-behavioural changes. AZA-PD is a clinical trial investigating the effects of the peripheral anti-inflammatory drug Azathioprine on PD progression, PET imaging via neuroinflammation via microglial activation ([11C]PK11195), s/f/dMRI hallmarks, blood/CSF cytokines, and behavioural measures of PD. This work is interested in peripheral and central nervous system inflammation being a principal driver of PD progression PDD, and the potential therapeutic targets for Parkinsonisms and dementia. Previously, my doctoral work supervised by Dr Emmanuel Stamatakis and advised by Prof David Menon focussed on the neurocognitive sequalae of chronic Traumatic Brain Injury (TBI), particularly the domains of response inhibition, working memory, executive function, and sustained attention – and how the pharmacological catecholaminergic stimulant Methylphenidate (MPh) ameliorates cognitive deficits by upregulating synaptic DA/NA concentrations. This research used both inside- and outside-scanner neuropsychological testing via the CANTAB cognitive assessments. This work also investigated their cognitive ability and psychiatric status using questionnaires including NART, MMSE, NPI, BDI, VAS, and SF-36. Both task-based and resting-state fMRI as well as DTI approaches were used to characterise the neurobiological underpinnings of TBI-deficits and MPh’s treatment effects compared to normative healthy control data. I collaborated with others in analysing patients with Disorders of Consciousness (DOC), the neurofunctional correlates of anaesthesia, and the effects of psychopharmacological modulators on resting-state fMRI data. TBI, DOC, and depressive conditions share neurological, behavioural, and cognitive deficits due to damage to monoaminergic structures.
