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Dr Yasir Ahmed Syed

Dr Yasir Ahmed Syed

Lecturer

School of Biosciences

Email
syedy@cardiff.ac.uk
Telephone
+44 (0)29 2068 8314
Campuses
Hadyn Ellis Building, Maindy Road, Cardiff, CF24 4HQ
Users
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. 

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.

Publications

2022

2021

2020

2019

2017

2016

2013

2011

2009

2008

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:

  1. BIT002 Research Techniques in Biosciences
  2. BI3451 Neurobiology of Brain Disorders
  3. BI3351 Contemporary Topics in Disease
  4. BI3001 Bioscience Final Year Project
  5. BI4001 Advanced Research Project
  6. BI4002 Advanced Research Methods
  7. BI9999 Professional Training Year.

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.

Supervision

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.

Past projects

Lead-Supervisor (70%) for Gareth Chapmann- Modelling of Neurodevelopmental Disorders Associated with 1q21.1 deletion and duplication using human iPSCs (awarded 2020).

Lead-Supervisor (70%) for Tanya Singh- Functional Role of 1q21.1 Chromosomal loci on the Development and Physiology of Neuro-immune Cells (submitted 2021).

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.