Ahmed Toosy's research has pursued the investigation of damage and recovery mechanisms from three independent major perspectives: 1) Anatomical– visual system with focus on optic neuropathies; 2) Pathological– with focus on demyelinating disorders; 3) Methodological – with the application of novel post-processing techniques such as connectivity analysis.

1) Visual system - With Alan Thompson,  he provided evidence for compensatory neuroplasticity and explored function-structure relationships after acute optic neuritis (Annals of Neurology and Human Brain Mapping). He described distributed functional changes after ischaemic optic neuropathy that were non-compensatory to clinical recovery (JNNP). He was involved in the APOSTEL recommendations for reporting recommendations of optical coherence tomography studies as part of the international IMSVISUAL collaboration (Neurology). He demonstrated  longitudinal trans-synaptic degeneration along the visual pathways after optic neuritis (Brain). He supported the phenytoin neuroprotection trial in acute optic neuritis (PI Raj Kapoor) and led the MRI component of the study. The results showed a beneficial effect of phenytoin on the degree of neuroaxonal loss of the optic nerve after optic neuritis (Lancet Neurology). He was the UK-PI for a pharmaceutically led study of high-dose biotin in chronic optic neuropathy (CNS Drugs). 

2) Demyelinating Disorders – By investigating potential MRI markers of structural damage, with Olga Ciccarelli, he has contributed to studies of advanced MRI techniques such as magnetisation transfer imaging and diffusion weighted MRI that have quantified microstructural injury in white matter and cerebellum in multiple sclerosis (Multiple Sclerosis Journal, Human Brain Mapping). Microstructural injury and metabolic dysfunction were also  quantified in the cervical cords of people with multiple sclerosis and neuromyelitis optica, another demyelinating disorder (Neurology, Annals Neurology, Journal Neuroscience). He has led on the recruitment and assessment on an ongoing longitudinal cohort of clinically isolated syndrome (very early multiple sclerosis) to determine early biomarkers and gain pathophysiological insights that can predict future disability. This has been supported by a recent MRC Research Grant award for a five year follow up of this cohort.

3) Methodological advances – the application of connectomics in multiple sclerosis disorders with Claudia Wheeler-Kingshott and Jonathan Clayden. This field uses graph theory to investigate structural and functional relationships between different cortical regions, treating the whole brain or one of its sub-systems as an integrated network. Structural cortical networks, derived from cortical thickness maps, have showed network alterations in clinically isolated syndromes in an international MAGNIMS collaboration and changes over time in those converting to multiple sclerosis (Sci Reports, Multiple Sclerosis Journal). Structural cortical network dynamics also switch from low to high efficiency in people with multiple sclerosis who progress faster (Multiple Sclerosis Journal). Diffusion-derived connectivity network analysis can also explain clinical disability better than conventional MRI measures of brain atrophy (JNNP). These findings demonstrate the potential of connectivity to provide valuable insights into brain network trajectories of clinical relevance.