PhD opportunities

• Does common genetic risk for schizophrenia shape brain anatomy and function?

Despite the assumption that common risk alleles for schizophrenia trigger brain changes that explain clinical symptoms, this association has not been clearly demonstrated. The lack of specificity in genomic approaches and the use of sub-optimal brain phenotypes have hindered progress. This project aims to implement innovative imaging and analytical methods to address this conundrum, potentially leading to improved diagnosis and new targets for treatment development.

Lead Supervisor: Dr Xavier Caseras

• Using a new translational in vivo model to understand the neurobiology underlying ADHD subtypes

In mice and humans loss-of-function of the steroid sulfatase (STS) enzyme results in inattention but enhanced motor response inhibition; we aim to understand the neurobiology underlying this dissociation using a new mouse model. The project will develop behavioural neuroscience research skills, will have direct clinical relevance to X-linked ichthyosis (STS deficiency), and will signpost mechanisms associated with Attention Deficit Hyperactivity Disorder subtypes.

Lead Supervisor: Dr William Davies

• Untangling neurodegeneration and ageing components of neuroinflammatory disorders

Numerous genome-wide association studies (GWAS) show a strong, but poorly understood neuroinflammatory component to most neurological diseases. This project will leverage such GWAS data from several neurological and inflammatory conditions to determine the relationships between immune system genes and underlying neurological pathologies and in addition to understanding the genetic influence of aging-dependent inflammatory changes.

Lead Supervisor: Prof Valentina Escott-Price

• Quantifying the molecular response to memory retrieval and its genetic association with schizophrenia

Deficits in the molecular mechanisms of memory are thought to be central to the psychiatric pathology associated with schizophrenia. New methods now allow us to explore deeper into the molecular dynamics of memory and refine our understanding of the impacts from schizophrenia. This interdisciplinary project aims to profile neuronal gene expression required for memory retrieval and extinction, and determine the molecular pathways of relevance to schizophrenia.

Lead Supervisor: Prof Jeremy Hall

• How does the schizophrenia candidate gene Sp4 influences transcription during neurodevelopment?

Common and rare variants in the gene encoding the neuronal transcription factor Sp4 have been linked to schizophrenia. This project explores how those variants alter the ability of Sp4 to regulate the activity of the genome. The student will gain a range of sophisticated in vivo, molecular biology, and bioinformatic techniques and apply these in order unravel the biology that links Sp4 to brain function, and identify what goes wrong in schizophrenia.

Lead Supervisor: Prof Anthony Isles

• What goes up must come down? Using digital technology to understand the dynamic nature of mood in bipolar disorder

People with bipolar disorder (BD) experience disabling episodes of high and low mood, but how mood fluctuates between episodes could provide key insights into the condition. This project will use long-term digital mood-monitoring data from the largest sample of people with BD in the world. The student will learn cutting-edge statistical methods to test if dynamic measures of mood are associated with clinical outcomes and genetic risk factors in people with BD.

Lead Supervisor: Dr Katie Lewis

• Investigating novel types of childhood irritability (emotional dysregulation) using a developmental and genetic approach

Severe childhood irritability is a common symptom across many mental health disorders and a common reason for mental health service referral. It is uncertain if irritability is a behavioural, neurodevelopmental or mood problem. This PhD will use longitudinal, population cohorts to examine irritability across development and test the hypothesis that there are different types of irritability, differentiated by developmental course, genetic and environmental aetiology.

Lead Supervisor: Dr Lucy Riglin
Institution: Cardiff

• The contribution of mitochondrial dysfunction to Alzheimer’s disease

Alzheimer’s disease (AD) is associated with increased oxidative stress and mitochondrial dysfunction in the brain. The Redox system that helps detoxify neurons is decreased in  AD patients and likely contributes to symptoms and neurodegeneration. The PhD student will manipulate Redox and mitochondrial regulating genes in Drosophila and iPSC neuron models of AD to find new potential therapeutic targets.

Lead Supervisor: Dr Gaynor Ann Smith

• Linking microRNA dynamics to mental health: Assessing the contribution of brain expressed miRNAs to the increased risk for psychiatric disorder in 22q11.2DS subjects

A large proportion of people with 22q11.2DS, a syndrome where a segment of DNA and associated genes are missing from chromosome 22, will fall ill with some form of psychiatric disorder. We suspect this increased risk for psychopathology is due to abnormalities in the brain metabolism of microRNAs. We will test this idea using patient-derived human neurons in partnership with Takeda who will provide support and a training secondment at the company in Tokyo, Japan.

Lead Supervisor: Prof Lawrence Wilkinson

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