Professor Ian Wood
- Position: Professor of Molecular Neuroscience
- Areas of expertise: Neuroscience; molecular biology; epigenetics; chromatin; gene expression; microglia; neurodegeneration
- Email: I.C.Wood@leeds.ac.uk
- Phone: +44(0)113 343 7922
- Location: G6.41c Garstang
- Website: Twitter | LinkedIn | Googlescholar | Researchgate | ORCID
Postdoctoral work at Scripps Research Institute, La Jolla, USA and University College, London, UK.
- Pro-Dean International
Epigenetics in chronic disease. We are interested in identifying the molecular mechanisms that are important in regulating gene transcription in human disease. Our work uses many molecular biological techniques, in vitro and in vivo model systems as well as clinical samples to provide a complete understanding of disease mechanisms.
Controlling excessive microglia activation: Activated microglia contribute to neuronal damage in neurodegenerative diseases and the neuronal damage observed after stroke and reperfusion. Activation of microglia and neuroinflammation is important in tissue repair but excessive inflammation is damaging and reducing such excess would provide therapeutic benefits. Chronic inflammation, predominantly mediated by microglial cells, is thought to play an important role in the progressive neuronal death seen in many neurological diseased states, including Alzheimer's disease (AD), Parkinson's disease (PD) and stroke. Identifying ways to reduce excessive microglia activation would thus provide therapeutic avenues for the development of new treatments for these debilitating neurological disorders. Our recently published data  have provided new insights into the ability of Histone deacetylase inhibitors to reduce microglia activation and we are currently working toward understanding the molecular mechanisms important in this response. Hopefully our work will provide a foundation for the development of new therapies that will have global impact.
 Inhibition of histone deacetylase 1 or 2 reduces induced cytokine expression in microglia through a protein synthesis independent mechanism. Durham BS, Grigg R, Wood IC. J Neurochem. 2017 Oct;143(2):214-224
Ageing and neurodegeneration: REST  is a transcription factor which represses the expression of around 2000 genes in the human genome, many of which are important for correct neuronal function. The expression of REST in neurons is low though the expression increases in normal human ageing and is thought to protect the neurons from oxidative stress and amyloid beta protein toxicity. Patients with Alzheimer’s disease or with mild cognitive impairment do not show an increased REST expression within the brain and a lack of REST in the neurons is associated with a susceptibility to stress and neurodegeneration. The mechanisms underlying the protective roles of REST are not known. We are currently investigating the mechanisms responsible for REST-mediated protection from stress using a range of molecular and genetic approaches.
 Chromatin crosstalk in development and disease: lessons from REST. Ooi L, Wood IC. Nat Rev Genet. 2007 Jul;8(7):544-54
Epilepsy: Epilepsy is the second most common neurological disorder affecting 1 in 130 people in the UK. Every day 100 new patients are diagnosed as epileptic and 1 in 20 people will suffer a seizure at some point in their lives. Neurones transmit signals via propagation of action potentials, the regulation of which is of utmost importance. One ion channel important in determining the excitability of neurones is the M-channel which is composed of subunits of the KCNQ potassium channel gene family. Mutations in KCNQ genes have been linked to heart disease, epilepsy, deafness and most recently pain . Despite their obvious importance, very little is known about how expression of these potassium channel genes is regulated though we do know that REST represses their expression  and NFAT enhance is . We are interested in determining how expression of these genes is regulated in normal physiology and in neuronal disorders such as epilepsy and chronic pain.
 Transcriptional repression of the M channel subunit Kv7.2 in chronic nerve injury. Rose K, Ooi L, Dalle C, Robertson B, Wood IC, Gamper N. Pain. 2011 Apr;152:742-54.
 Transcriptional control of KCNQ channel genes and the regulation of neuronal excitability. Mucha M, Ooi L, Linley JE, Mordaka P, Dalle C, Robertson B, Gamper N, Wood IC. J Neurosci. 2010 Oct 6;30:13235-45<h4>Research projects</h4> <p>Any research projects I'm currently working on will be listed below. Our list of all <a href="https://biologicalsciences.leeds.ac.uk/dir/research-projects">research projects</a> allows you to view and search the full list of projects in the faculty.</p>
- BSc, Imperial; PhD University College, London.
- Biochemical Society
Undergraduate project topics:
- Projects in all of the above areas are available for BSC and MBiol projects. Enthusiastic and committed students are encouraged to make specific enquiries.
- Students interested in applying for summer studentships should send an appropriate CV and cover letter
Postgraduate studentship areas:
- Applications are welcome from enthusiastic, committed students and postdocs to work on any of the above projects
Research groups and institutes
- Molecular Neuroscience