Dr Yasir Ahmed Syed
Lecturer
School of Biosciences
- SyedY@cardiff.ac.uk
- +44 29206 88314
- Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ
- Available for postgraduate supervision
Overview
The overarching goal of my lab is to define the key celluar and molecular pathways in the pathogenesis of neurodevelopmental and neuropsychiatric disorders. To gain a better insight into pathogenesis of these debilitating neurological disorders, such as Autism Spectrum Disorders (ASD), mood disorders, schizophrenia and white matter disorders, we use patient derived pluripotent stem cells and differentiate them into multiple neural linage cells and organoids in vitro. We employ combination of cellular, genetic, electrophysiological, behavioural and material science approaches to understand the mechanisms of disease initiation and progression, as to ultimately develop novel and reliable drug targets.
Complementary projects focuses on role of neuroinflammation and altered myelin development in the pathogenesis of neurodevelopmental disorders and psychiatric phenotypes.
Publication
2023
- Koceski, A., Smith, C., Syed, Y. A. and Trajkovski, V. 2023. Understanding the relationship between distress behaviour and health status of people with autism spectrum disorder. Healthcare
2022
- Robinson, J. et al. 2022. The association of neurodevelopmental abnormalities, congenital heart and renal defects in a Tuberous Sclerosis Complex patient cohort. BMC Medicine 20, article number: 123. (10.1186/s12916-022-02325-0)
- Dash, S., Syed, Y. A. and Khan, M. R. 2022. Understanding the role of the gut microbiome in brain development and its association with neurodevelopmental psychiatric disorders. Frontiers in Cell and Developmental Biology 10, article number: 880544. (10.3389/fcell.2022.880544)
- Chapman, G. et al. 2022. Using induced pluripotent stem cells to investigate human neuronal phenotypes in 1q21.1 deletion and duplication syndrome. Molecular Psychiatry 27, pp. 819-830. (10.1038/s41380-021-01182-2)
2021
- Dowden, L., Tucker, D., Morgan, S., Uzun, O. and Syed, Y. A. 2021. Contribution of congenital heart disorders associated with copy number variants in mediating risk for brain developmental disorders; evidence from 20-year retrospective cohort study. Frontiers in Cardiovascular Medicine 8, article number: 655463. (10.3389/fcvm.2021.655463)
2020
- Akter, F., Yu, X., Qin, X., Yao, S., Nikrouz, P., Syed, Y. A. and Kotter, M. 2020. Corrigendum: The pathophysiology of degenerative cervical myelopathy and the physiology of recovery following decompression. Frontiers in Neuroscience 14, pp. 628. (10.3389/fnins.2020.00628)
- Drakulic, D. et al. 2020. Copy number variants (CNVs): a powerful tool for iPSC-based modelling of ASD. Molecular Autism 11(1), article number: 42. (10.1186/s13229-020-00343-4)
- Akter, F., Yu, X., Qin, X., Yao, S., Nikrouz, P., Syed, Y. and Kotter, M. 2020. The pathophysiology of degenerative cervical myelopathy and the physiology of recovery following decompression. Frontiers in Neuroscience 14, article number: 138. (10.3389/fnins.2020.00138)
- Savory, K., Manivannan, S., Zaben, M., Uzun, O. and Syed, Y. A. 2020. Impact of copy number variation on human neurocognitive deficits and congenital heart defects: a systematic review. Neuroscience and Biobehavioral Reviews 108, pp. 83-93. (10.1016/j.neubiorev.2019.10.020)
- Savory, K. and Syed, Y. A. 2020. Advances in the understanding of cellular pathogenesis associated with Autism Spectrum Disorder. Journal for ReAttach Therapy and Developmental Diversities 2(2), pp. 96-118.
2019
- Silva, A. I. et al. 2019. Cyfip1 haploinsufficient rats show white matter changes, myelin thinning, abnormal oligodendrocytes and behavioural inflexibility. Nature Communications 10, article number: 3455. (10.1038/s41467-019-11119-7)
2017
- Radtke, F., Chapman, G., Hall, J. and Syed, Y. A. 2017. Modulating neuroinflammation to treat neuropsychiatric disorders. BioMed Research International, article number: 5071786.
2016
- Syed, Y. A., Abdulla, S. A. and Kotter, M. R. N. 2016. Studying the effects of semaphorins on oligodendrocyte lineage cells. In: Terman, J. R. ed. Semaphorin Signaling., Vol. 1493. Methods in Molecular Biology New York, NY: Humana Press, pp. 363-378., (10.1007/978-1-4939-6448-2_26)
- Gonzalez, G. A. et al. 2016. Tamoxifen accelerates the repair of demyelinated lesions in the central nervous system. Scientific Reports 6, article number: 31599. (10.1038/srep31599)
- Dhillon, R. S. et al. 2016. Axonal plasticity underpins the functional recovery following surgical decompression in a rat model of cervical spondylotic myelopathy. Acta Neuropathologica Communications 4, article number: 89. (10.1186/s40478-016-0359-7)
- Syed, Y. A. et al. 2016. Antibody-mediated neutralization of myelin-associated EphrinB3 accelerates CNS remyelination. Acta Neuropathologica 131(2), pp. 281-298. (10.1007/s00401-015-1521-1)
2013
- Syed, Y. A. et al. 2013. Inhibition of phosphodiesterase-4 promotes oligodendrocyte precursor cell differentiation and enhances CNS remyelination. EMBO Molecular Medicine 5(12), pp. 1918-1934. (10.1002/emmm.201303123)
- Hannan, N. et al. 2013. Generation of multipotent foregut stem cells from human pluripotent stem cells. Stem Cell Reports 1(4), pp. 293-306. (10.1016/j.stemcr.2013.09.003)
2011
- Syed, Y. A., Hand, E., Mobius, W., Zhao, C., Hofer, M., Nave, K. A. and Kotter, M. R. 2011. Inhibition of CNS remyelination by the presence of semaphorin 3A. Journal of Neuroscience 31(10), pp. 3719-3728. (10.1523/JNEUROSCI.4930-10.2011)
2009
- Baer, A. S. et al. 2009. Myelin-mediated inhibition of oligodendrocyte precursor differentiation can be overcome by pharmacological modulation of Fyn-RhoA and protein kinase C signalling. Brain 132(2), pp. 465-481. (10.1093/brain/awn334)
2008
- Syed, Y. A., Baer, A. S., Lubec, G., Hoeger, H., Widhalm, G. and Kotter, M. R. 2008. Inhibition of oligodendrocyte precursor cell differentiation by myelin-associated proteins. Neurosurgical Focus 24(3-4), article number: E5. (10.3171/FOC/2008/24/3-4/E4)
Articles
- Koceski, A., Smith, C., Syed, Y. A. and Trajkovski, V. 2023. Understanding the relationship between distress behaviour and health status of people with autism spectrum disorder. Healthcare
- Robinson, J. et al. 2022. The association of neurodevelopmental abnormalities, congenital heart and renal defects in a Tuberous Sclerosis Complex patient cohort. BMC Medicine 20, article number: 123. (10.1186/s12916-022-02325-0)
- Dash, S., Syed, Y. A. and Khan, M. R. 2022. Understanding the role of the gut microbiome in brain development and its association with neurodevelopmental psychiatric disorders. Frontiers in Cell and Developmental Biology 10, article number: 880544. (10.3389/fcell.2022.880544)
- Chapman, G. et al. 2022. Using induced pluripotent stem cells to investigate human neuronal phenotypes in 1q21.1 deletion and duplication syndrome. Molecular Psychiatry 27, pp. 819-830. (10.1038/s41380-021-01182-2)
- Dowden, L., Tucker, D., Morgan, S., Uzun, O. and Syed, Y. A. 2021. Contribution of congenital heart disorders associated with copy number variants in mediating risk for brain developmental disorders; evidence from 20-year retrospective cohort study. Frontiers in Cardiovascular Medicine 8, article number: 655463. (10.3389/fcvm.2021.655463)
- Akter, F., Yu, X., Qin, X., Yao, S., Nikrouz, P., Syed, Y. A. and Kotter, M. 2020. Corrigendum: The pathophysiology of degenerative cervical myelopathy and the physiology of recovery following decompression. Frontiers in Neuroscience 14, pp. 628. (10.3389/fnins.2020.00628)
- Drakulic, D. et al. 2020. Copy number variants (CNVs): a powerful tool for iPSC-based modelling of ASD. Molecular Autism 11(1), article number: 42. (10.1186/s13229-020-00343-4)
- Akter, F., Yu, X., Qin, X., Yao, S., Nikrouz, P., Syed, Y. and Kotter, M. 2020. The pathophysiology of degenerative cervical myelopathy and the physiology of recovery following decompression. Frontiers in Neuroscience 14, article number: 138. (10.3389/fnins.2020.00138)
- Savory, K., Manivannan, S., Zaben, M., Uzun, O. and Syed, Y. A. 2020. Impact of copy number variation on human neurocognitive deficits and congenital heart defects: a systematic review. Neuroscience and Biobehavioral Reviews 108, pp. 83-93. (10.1016/j.neubiorev.2019.10.020)
- Savory, K. and Syed, Y. A. 2020. Advances in the understanding of cellular pathogenesis associated with Autism Spectrum Disorder. Journal for ReAttach Therapy and Developmental Diversities 2(2), pp. 96-118.
- Silva, A. I. et al. 2019. Cyfip1 haploinsufficient rats show white matter changes, myelin thinning, abnormal oligodendrocytes and behavioural inflexibility. Nature Communications 10, article number: 3455. (10.1038/s41467-019-11119-7)
- Radtke, F., Chapman, G., Hall, J. and Syed, Y. A. 2017. Modulating neuroinflammation to treat neuropsychiatric disorders. BioMed Research International, article number: 5071786.
- Gonzalez, G. A. et al. 2016. Tamoxifen accelerates the repair of demyelinated lesions in the central nervous system. Scientific Reports 6, article number: 31599. (10.1038/srep31599)
- Dhillon, R. S. et al. 2016. Axonal plasticity underpins the functional recovery following surgical decompression in a rat model of cervical spondylotic myelopathy. Acta Neuropathologica Communications 4, article number: 89. (10.1186/s40478-016-0359-7)
- Syed, Y. A. et al. 2016. Antibody-mediated neutralization of myelin-associated EphrinB3 accelerates CNS remyelination. Acta Neuropathologica 131(2), pp. 281-298. (10.1007/s00401-015-1521-1)
- Syed, Y. A. et al. 2013. Inhibition of phosphodiesterase-4 promotes oligodendrocyte precursor cell differentiation and enhances CNS remyelination. EMBO Molecular Medicine 5(12), pp. 1918-1934. (10.1002/emmm.201303123)
- Hannan, N. et al. 2013. Generation of multipotent foregut stem cells from human pluripotent stem cells. Stem Cell Reports 1(4), pp. 293-306. (10.1016/j.stemcr.2013.09.003)
- Syed, Y. A., Hand, E., Mobius, W., Zhao, C., Hofer, M., Nave, K. A. and Kotter, M. R. 2011. Inhibition of CNS remyelination by the presence of semaphorin 3A. Journal of Neuroscience 31(10), pp. 3719-3728. (10.1523/JNEUROSCI.4930-10.2011)
- Baer, A. S. et al. 2009. Myelin-mediated inhibition of oligodendrocyte precursor differentiation can be overcome by pharmacological modulation of Fyn-RhoA and protein kinase C signalling. Brain 132(2), pp. 465-481. (10.1093/brain/awn334)
- Syed, Y. A., Baer, A. S., Lubec, G., Hoeger, H., Widhalm, G. and Kotter, M. R. 2008. Inhibition of oligodendrocyte precursor cell differentiation by myelin-associated proteins. Neurosurgical Focus 24(3-4), article number: E5. (10.3171/FOC/2008/24/3-4/E4)
Book sections
- Syed, Y. A., Abdulla, S. A. and Kotter, M. R. N. 2016. Studying the effects of semaphorins on oligodendrocyte lineage cells. In: Terman, J. R. ed. Semaphorin Signaling., Vol. 1493. Methods in Molecular Biology New York, NY: Humana Press, pp. 363-378., (10.1007/978-1-4939-6448-2_26)
- Syed, Y. A., Abdulla, S. A. and Kotter, M. R. N. 2016. Studying the effects of semaphorins on oligodendrocyte lineage cells. In: Terman, J. R. ed. Semaphorin Signaling., Vol. 1493. Methods in Molecular Biology New York, NY: Humana Press, pp. 363-378., (10.1007/978-1-4939-6448-2_26)
- Gonzalez, G. A. et al. 2016. Tamoxifen accelerates the repair of demyelinated lesions in the central nervous system. Scientific Reports 6, article number: 31599. (10.1038/srep31599)
- Dhillon, R. S. et al. 2016. Axonal plasticity underpins the functional recovery following surgical decompression in a rat model of cervical spondylotic myelopathy. Acta Neuropathologica Communications 4, article number: 89. (10.1186/s40478-016-0359-7)
- Syed, Y. A. et al. 2016. Antibody-mediated neutralization of myelin-associated EphrinB3 accelerates CNS remyelination. Acta Neuropathologica 131(2), pp. 281-298. (10.1007/s00401-015-1521-1)
- Syed, Y. A., Baer, A. S., Lubec, G., Hoeger, H., Widhalm, G. and Kotter, M. R. 2008. Inhibition of oligodendrocyte precursor cell differentiation by myelin-associated proteins. Neurosurgical Focus 24(3-4), article number: E5. (10.3171/FOC/2008/24/3-4/E4)
Research
Neurodevelopmental disorders and psychiatric disorders are common, debilitating disorders including autism, intellectual disability, and perhaps even schizophrenia. These disorders can have deep consequences on different dimensions of the individual including social and emotional. Recent genetic findings have identified mutations including alteration at chromosomal locus of 1q21.1, 3q29 and 16p11.2 which significantly increases risk for these multiple disorders across life span. How these risk factors contribute to impaired brain development and functionality is poorly understood. My research has been focused on identifying the neurobiological basis of genetic risk factors of neurodevelopmental disorders and psychiatric diseases with the intention of identifying specific drug targets for future therapeutic interventions of these devastating brain disorders.
Research in the lab focuses on the following objectives:
Defining neural and molecular basis of microcephaly and macrocephaly: Human microcephaly and macrocephaly refer to aberrant neurodevelopmental conditions associated with smaller or bigger heads as compared to babies of same age and gender. They are present at birth or can develop postnatally. Infants associated with these disorders are at greater risk for long term morbidity such as behavioural abnormalities, developmental delay, seizures, motor impairment and problems with eyesight and hearing. What causes the peculiar pattern of human brain growth is as yet unknow, limiting the effort to develop the effective treatments. Subjects with gene dosage alterations either due to gains or deletions of genetic material at human chromosome 1q21.1 locus are strongly associated with micro or macrocephalus condition. The locus consists of several key genes such as HYDIN2, NOTCH2NL which have been suggested to control the brain size and proliferation efficiency of the neuronal cells. Studying the impact of 1q21.1 deletion and duplication on brain development promises to dissect the neural pathology and dysregulated molecular mechanisms associated with aberrant brain development. We have generated induced pluripotent stem cells from individuals with 1q21.1 deletion or duplication and differentiated them into “cortical organoids” or “mini brains”. As these organoids display an architecture and neural network activity resembling that of human brain tissue, we are using them to identity defects in cortex formation, neural cell proliferation and differentiation.
Mechanisms of white matter changes in the neurodevelopmental disorder and mental illness: Disruptions of white matter microstructure have been widely reported in the broad range of neurodevelopmental disorders and psychiatric diseases. However, the emergence of these alterations and the underlying cellular mechanism during preclinical stages and chronic phase of disease remains poorly understood. Using genetic risk variant-16p11.2 deletion and duplications as prototype examples, which is associated with increased risk for autism and multiple psychiatric conditions, we are employing cutting-edge stem cell approaches including 2D and 3D models of developmental myelination to investigatie the molecular basis of altered developmental myelination. Understanding these specific biological processes disrupted in presence of genetic risk variant may provide a molecular window into key neurodevelopmental processes relevant to neuropsychiatric phenotypes.
Contribution of neuroinflammation on brain development: Clinical and experimental data provide evidence that the perinatal exposure to inflammatory factors can alter the programs of brain development leading to neurodevelopmental and psychiatric clinical phenotypes. It is remains unclear if the presence of genetic risk factors contributes to altered inflammatory pathways leading to abnormal brain development. To address this, we are using iPSC derived astrocytes and microglia from subjects carrying high risk genetic variants to identify any altered developmental program and its effect on functionality of neurons.
Research team members
- Emma Weir
- Kübra Trabzonlu
- Isabelle Harris.
Teaching
I teach both postgraduate and undergraduate modules. I also supervise final year undergraduate and postgraduate dissertation topics that broadly fall within the developmental neuroscience and cellular biology remit.
In 2021-22, I am contributing to the following modules:
- BIT002 Research Techniques in Biosciences
- BI3451 Neurobiology of Brain Disorders
- BI3351 Contemporary Topics in Disease
- BI3001 Bioscience Final Year Project
- BI4001 Advanced Research Project
- BI4002 Advanced Research Methods
- BI9999 Professional Training Year.
Biography
Academic positions
- Lecturer in Neuroscience: School of Biosciences, Cardiff University, Cardiff
- Group Leader: Neuroscience and Mental Health Institute, Cardiff University, Cardiff
- Postdoctoral Research Associate: Welcome Trust-MRC Cambridge Stem Cell Institute, University of Cambridge, UK
- PhD: Max-Planck Institute for Experimental Medicine, Germany and Medical University of Vienna, Austria.
Professional memberships
- The Higher Education Academy (FHEA)
- Research Committee, Cardiff Institute for Tissue Engineering and Repair (CITER)
- Genetics Society, UK
- International Society for Stem Cell Research.
Committees and reviewing
Editorial board member
- Frontiers in Neuroscience
- BMC Neurosceince
- Biomed Reseaarch International
- Journal for Reattach Therapy and Developmental Diversities.
Grant reviewer
- MRC
- ERC
- British council-Newton fund
- UK MS Society.
Supervisions
I am interested in supervising PhD students in the areas of:
- Neuron and Glial Cell Biology
- Neurodevelopmental Psychiatric disorders
- Neuroinflammation
- 3D Bioprinting
- Heart-Brain developmental axis.
Interested in discussing ideas/ joining my lab as postgraduate student/postdoc, please contact me by email.
Engagement
Some recent engagement activities include:
- Judge: British Brain Bee (Neuroscience Olympiad for teenagers)
- Speaker: Awakening Oligodendrocyte Precursor, The Scientist
- Patient focused meeting-UK MS Society.