Mr Darren Cameron
Research Associate, Division of Psychological Medicine and Clinical Neurosciences
- CameronD@cardiff.ac.uk
- Hadyn Ellis Building, Room 2.01 - Desk 46, Maindy Road, Cardiff, CF24 4HQ
Publication
2023
- Cameron, D. et al. 2023. Single nuclei RNA sequencing of 5 regions of the human prenatal brain implicates developing neuron populations in genetic risk for schizophrenia. Biological Psychiatry 93, pp. 157-166. (10.1016/j.biopsych.2022.06.033)
2021
- Kouakou, M., Cameron, D., Hannon, E., Dempster, E. L., Mill, J., Hill, M. J. and Bray, N. 2021. Sites of active gene regulation in the prenatal frontal cortex and their role in neuropsychiatric disorders. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 186(6), pp. 376-388. (10.1002/ajmg.b.32877)
2019
- Cameron, D., Blake, D. J., Bray, N. J. and Hill, M. J. 2019. Transcriptional changes following cellular knockdown of the schizophrenia risk gene SETD1A are enriched for common variant association with the disorder. Molecular Neuropsychiatry 5(2), pp. 109-114. (10.1159/000497181)
- Cameron, D. 2019. Gene regulation in microglia and genetic risk for complex brain disorders. PhD Thesis, Cardiff University.
2018
- Pardinas, A. F. et al. 2018. Common schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection. Nature Genetics 50, pp. 381-389. (10.1038/s41588-018-0059-2)
- Tansey, K. E., Cameron, D. and Hill, M. J. 2018. Genetic risk for Alzheimer's disease is concentrated in specific macrophage and microglial transcriptional networks. Genome Medicine 10, article number: 14. (10.1186/s13073-018-0523-8)
2017
- Clifton, N., Cameron, D., Trent, S., Sykes, L. H., Thomas, K. L. and Hall, J. 2017. Hippocampal regulation of postsynaptic density Homer1 by associative learning. Neural Plasticity 2017, article number: 5959182. (10.1155/2017/5959182)
2016
- Pardinas, A. et al. 2016. Common schizophrenia alleles are enriched in mutation-intolerant genes and maintained by background selection. [Online]. bioRxiv. (10.1101/068593) Available at: http://dx.doi.org/10.1101/068593
Articles
- Cameron, D. et al. 2023. Single nuclei RNA sequencing of 5 regions of the human prenatal brain implicates developing neuron populations in genetic risk for schizophrenia. Biological Psychiatry 93, pp. 157-166. (10.1016/j.biopsych.2022.06.033)
- Kouakou, M., Cameron, D., Hannon, E., Dempster, E. L., Mill, J., Hill, M. J. and Bray, N. 2021. Sites of active gene regulation in the prenatal frontal cortex and their role in neuropsychiatric disorders. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 186(6), pp. 376-388. (10.1002/ajmg.b.32877)
- Cameron, D., Blake, D. J., Bray, N. J. and Hill, M. J. 2019. Transcriptional changes following cellular knockdown of the schizophrenia risk gene SETD1A are enriched for common variant association with the disorder. Molecular Neuropsychiatry 5(2), pp. 109-114. (10.1159/000497181)
- Pardinas, A. F. et al. 2018. Common schizophrenia alleles are enriched in mutation-intolerant genes and in regions under strong background selection. Nature Genetics 50, pp. 381-389. (10.1038/s41588-018-0059-2)
- Tansey, K. E., Cameron, D. and Hill, M. J. 2018. Genetic risk for Alzheimer's disease is concentrated in specific macrophage and microglial transcriptional networks. Genome Medicine 10, article number: 14. (10.1186/s13073-018-0523-8)
- Clifton, N., Cameron, D., Trent, S., Sykes, L. H., Thomas, K. L. and Hall, J. 2017. Hippocampal regulation of postsynaptic density Homer1 by associative learning. Neural Plasticity 2017, article number: 5959182. (10.1155/2017/5959182)
Thesis
- Cameron, D. 2019. Gene regulation in microglia and genetic risk for complex brain disorders. PhD Thesis, Cardiff University.
Websites
- Pardinas, A. et al. 2016. Common schizophrenia alleles are enriched in mutation-intolerant genes and maintained by background selection. [Online]. bioRxiv. (10.1101/068593) Available at: http://dx.doi.org/10.1101/068593
Biography
My research focuses on the analysis and interpretation of single cell genomics data and their integration with data from neuropsychiatric disorder GWAS to identify the cell types and molecular mechanisms that mediate risk for complex brain disorders.