Connor Scott is a neuroscientist with over 8 years of human tissue experience, specialising in bringing traditional histology into the modern era by developing workflows to bridge neuropathology with multiple ‘omic’ technologies using surgical and post-mortem CNS material.
Scroll down to see a brief overview of his academic profile or click on the headings above to get a more in-depth view.
D.Phil (Oxon) in Clinical Neurosciences, (current)
University of Oxford
BSc (Hons) in Biomedical Sciences, 2012
University of Greenwich
Senior Research Scientist.
Current projects: (1) selective vulnerability in amyotrophic lateral sclerosis, (2) early detection of Alzheimer’s Disease, (3) novel biomarker discovery in Alzheimer’s disease, (4) microproteomics of rare neuronal cell types/tumour samples, (5) genetic classification of gliomas, (6) High-resolution MRI scanning.
Establishing, managing, and maintaining several core research facilities within NDCN. This includes providing training and troubleshooting.
Facilities: Whole Slide Digital Imaging, Automated IHC/ISH and Laser Microdissection.
Day to day advisory role for post-graduates (MSc, MRes, D.Phil) and post-doctoral scientists.
Specialized training to students (undergraduates/postgraduates) and professionals (laboratory technicians, research assistants, post-doctoral researchers).
Supervisory role on several FHS research projects; both for medical students and undergraduates. Experience managing students, determining project direction, placing deadlines, managing student concerns, and helping students reach their targets.
Click Employment Experience for a detailed summary.
Degeneration of the primary motor cortex is a defining feature of amyotrophic lateral sclerosis (ALS), which is associated with the accumulation of microscopic protein aggregates in neurons and glia. However, little is known about the quantitative burden and pattern of motor cortex proteinopathies across ALS genotypes. We combined quantitative digital image analysis with multi-level generalized linear modelling in an independent cohort of 82 ALS cases to explore the relationship between genotype, total proteinopathy load and cellular vulnerability to aggregate formation. Primary motor cortex phosphorylated (p)TDP-43 burden and microglial activation were more severe in sporadic ALS-TDP disease than C9-ALS. Oligodendroglial pTDP-43 pathology was a defining feature of ALS-TDP in sporadic ALS, C9-ALS and ALS with OPTN, HNRNPA1 or TARDBP mutations. ALS-FUS and ALS-SOD1 showed less cortical proteinopathy in relation to spinal cord pathology than ALS-TDP, where pathology was more evenly spread across the motor cortex-spinal cord axis. Neuronal pTDP-43 aggregates were rare in GAD67+ and Parvalbumin+ inhibitory interneurons, consistent with predominant accumulation in excitatory neurons. Finally, we show that cortical microglia, but not astrocytes, contain pTDP-43. Our findings suggest divergent quantitative, genotype-specific vulnerability of the ALS primary motor cortex to proteinopathies, which may have implications for our understanding of disease pathogenesis and the development of genotype-specific therapies.
Developing a technique that allows for differential quantitative proteomic analysis to be performed on minute amount of post-mortem laser microdissected material.