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Neuroscience
|MPhil/PhD
|Part Time, Full Time
Staff interests associated with the research programme and its research groups
The Centre for the Cellular Basis of Behaviour (CCBB) opened in January 2007 and is part of the Department of Neuroscience at the Institute of Psychiatry.
The objectives of the CCBB are to:
The principle areas of research in the CCBB are:
Many of the members of the CCBB are also members of the the Department of Neuroscience and the MRC Centre for Neurodegeneration Research (CNR).
The objectives of the CCBB are to:
- Substantially increase the Institute’s research capacity in Basic and Clinical Neuroscience.
- Open new areas of research into the neurobiological basis of neurodegenerative and psychiatric disease.
- Strengthen and create collaborative opportunities with King’s Medical School.
- Provide a focus for scientific excellence on the Denmark Hill Campus.
The principle areas of research in the CCBB are:
- Neural Stem Cells
- Molecular Neurobiology
- The Neurobiology of Mental Health
The following research groups collectively form the Centre for the Cellular Basis of Behaviour.
Further information about the research activities of the following Principal Investigators can be found by clicking on the links below.
- Nick Bray (Neurobiology of Schizophrenia)
- Noel Buckley (Molecular Neuroscience)
- Jon Cooper (Pediatric Storage Disorders Laboratory & Batten Disease)
- Karl Peter Giese (Molecular Analysis of Memory)
- Mike Modo (Stem Cell Imaging Laboratory)
- Carmine Pariante (Stress, Psychiatry and Immunology Laboratory)
- Jack Price (Neural Stem Cell Biology)
- Yuh-Man Sun (Molecular Mechanisms of Neural Stem Cell Development)
- Sandrine Thuret (Nutrition, Neurogenesis and Mental Health)
- Dafe Uwanogho (Neural Stem Cell Genomics)
- Brenda Williams (Biology of Neural Stem Cells and Neural Progenitor Cells).
Many of the members of the CCBB are also members of the the Department of Neuroscience and the MRC Centre for Neurodegeneration Research (CNR).
Website:
The CNR particularly focuses on two neurodegenerative diseases: Alzheimer's disease and motor neurone disease. Over half a million people have Alzheimer's disease in the UK and this number is likely to rise with the increase in the elderly population. It is therefore important that there is a much better understanding of the causes of the disease in order to develop more effective therapeutic strategies.
It is estimated that there are up to 5,000 people with motor neurone disease in the UK. In the majority of cases (more than 90 per cent), the diseases appear for no apparent reason (sporadic form) but the remaining cases occur in families (familial form) indicating that inherited genetic factors are involved. These cases are especially important because they provide clues of factors that can give rise to the diseases.
The centre brings together scientists investigating the causative mechanisms of these conditions in the laboratory with clinical colleagues investigating patients and conducting clinical trials. The combined laboratory and clinical investigations are aimed at identifying new therapeutic targets for drugs can be developed to find better treatments as well as to develop laboratory-based diagnostic methods.
The centre also includes stem cell research since this is an alternative possible treatment and state-of-the-art neuroimaging research, neuropsychology, epidemiological research and genetics, all of which are essential for improving our understanding of these conditions and monitoring the effectiveness of new drugs. The centre will work closely with the South London and Maudsley NHS Trust (SLAM), the King's College Hospital NHS Trust (KCH) and Proteome Sciences plc.
It is estimated that there are up to 5,000 people with motor neurone disease in the UK. In the majority of cases (more than 90 per cent), the diseases appear for no apparent reason (sporadic form) but the remaining cases occur in families (familial form) indicating that inherited genetic factors are involved. These cases are especially important because they provide clues of factors that can give rise to the diseases.
The centre brings together scientists investigating the causative mechanisms of these conditions in the laboratory with clinical colleagues investigating patients and conducting clinical trials. The combined laboratory and clinical investigations are aimed at identifying new therapeutic targets for drugs can be developed to find better treatments as well as to develop laboratory-based diagnostic methods.
The centre also includes stem cell research since this is an alternative possible treatment and state-of-the-art neuroimaging research, neuropsychology, epidemiological research and genetics, all of which are essential for improving our understanding of these conditions and monitoring the effectiveness of new drugs. The centre will work closely with the South London and Maudsley NHS Trust (SLAM), the King's College Hospital NHS Trust (KCH) and Proteome Sciences plc.
Website:
The Department of Neuroscience consists of the Section of Neuroscience and the Centre for the Cellular Basis of Behavior. It also hosts the MRC Centre for Neurodegeneration Research. Professor Noel Buckley is the head of the Department of Neuroscience.
The main focus of the Section of Neuroscience’s research is to further understanding of the molecular basis of neurodegeneration, focusing on the way the brain degenerates in Alzheimer’s disease, Parkinson’s disease, motor neurone disease, and the transmissible spongiform encephalopathies.
The CCBB also carries out research in these areas, such as Batten disease, and additionally carries out research on neural stem cells and on the neurobiology of mental health, especially on understanding the cellular organisation of the cerebral cortex in relation to the neurodevelopmental hypotheses of schizophrenia.
For more details, please refer to http://www.iop.kcl.ac.uk/departments/?locator=7&context=research
Our principal achievements have centred around (1) derivation, characterisation and application of neural stem cells and (2) understanding genetic and molecular mechanisms that underlie neurodegenerative and psychiatric disorders. We have uncovered genetic and epigenetic pathways regulating neural stem cell renewal in model organisms such as fly and mouse and used transplantation studies to examine efficacy of neural stem cells in animal models of stroke and Huntington’s Disease (HD). Notably, this has led to the first association between in vivo MRI-based anatomical measurements and their prediction of behavioural improvements in stroke. Further, we have pioneered the use of human neural stem cells for treatment of stroke and have produced the first clinical grade human neural stem cell lines, currently entering clinical trials for stroke. Another trailblazer is the first clinical trial of human neural stem cells in a neurodegenerative disorder (Batten Disease). Further efforts are aimed at understanding the mechanisms by which diet modulates adult hippocampal neurogenesis and the subsequent impact on mental health. Other breakthroughs include the demonstration that similar impairments of synaptic signalling may underlie both early Alzheimer’s disease (AD) and schizophrenia (SZ), providing a novel linkage between seemingly disparate disorders. Further progress continues to be made into fundamental genetic and molecular mechanisms underlying neurodegenerative disorders and psychiatric disorders, particularly with regard to understanding susceptibility gene expression in SZ and the role of ß-amyloid in AD. HD is also in our sights, and we have carried out the first whole-genome study of aberrant transcription factor binding in HD brain and examined the therapeutic potential of neural stem cell transplantation in animal models of HD.
The Department of Neuroscience is involved in several collaborations, across the globe, including collaborators in the US (Columbia University, Washington University, Penn University, UCLA, UCSD), Australasia (Lincoln University, University of Sydney), Europe (Universities of Milan, Rome, Naples Helsinki, Freiburg) and Asia (The Genome Institute of Singapore). We also have many collaborations within the UK including Universities of Oxford, Cambridge, Nottingham, and also with ReNeuron, a UK biotech company focusing on stem-cell therapy.
The department participates in a BSc (Intercalated) in Neuroscience and Neuropsychology pathway.
The department also runs one taught MSc course in Neuroscience. This Masters degree is offered as a one-year full-time programme and as a two-year part-time programme; it provides specialised pathways in Addiction Biology, Developmental Neurobiology, Neurodegeneration, Neuroimaging and Cognitive Neuroscience
For those wishing for supervision in doing a PhD, current vacancies can be found here.
The main focus of the Section of Neuroscience’s research is to further understanding of the molecular basis of neurodegeneration, focusing on the way the brain degenerates in Alzheimer’s disease, Parkinson’s disease, motor neurone disease, and the transmissible spongiform encephalopathies.
The CCBB also carries out research in these areas, such as Batten disease, and additionally carries out research on neural stem cells and on the neurobiology of mental health, especially on understanding the cellular organisation of the cerebral cortex in relation to the neurodevelopmental hypotheses of schizophrenia.
For more details, please refer to http://www.iop.kcl.ac.uk/departments/?locator=7&context=research
Our principal achievements have centred around (1) derivation, characterisation and application of neural stem cells and (2) understanding genetic and molecular mechanisms that underlie neurodegenerative and psychiatric disorders. We have uncovered genetic and epigenetic pathways regulating neural stem cell renewal in model organisms such as fly and mouse and used transplantation studies to examine efficacy of neural stem cells in animal models of stroke and Huntington’s Disease (HD). Notably, this has led to the first association between in vivo MRI-based anatomical measurements and their prediction of behavioural improvements in stroke. Further, we have pioneered the use of human neural stem cells for treatment of stroke and have produced the first clinical grade human neural stem cell lines, currently entering clinical trials for stroke. Another trailblazer is the first clinical trial of human neural stem cells in a neurodegenerative disorder (Batten Disease). Further efforts are aimed at understanding the mechanisms by which diet modulates adult hippocampal neurogenesis and the subsequent impact on mental health. Other breakthroughs include the demonstration that similar impairments of synaptic signalling may underlie both early Alzheimer’s disease (AD) and schizophrenia (SZ), providing a novel linkage between seemingly disparate disorders. Further progress continues to be made into fundamental genetic and molecular mechanisms underlying neurodegenerative disorders and psychiatric disorders, particularly with regard to understanding susceptibility gene expression in SZ and the role of ß-amyloid in AD. HD is also in our sights, and we have carried out the first whole-genome study of aberrant transcription factor binding in HD brain and examined the therapeutic potential of neural stem cell transplantation in animal models of HD.
The Department of Neuroscience is involved in several collaborations, across the globe, including collaborators in the US (Columbia University, Washington University, Penn University, UCLA, UCSD), Australasia (Lincoln University, University of Sydney), Europe (Universities of Milan, Rome, Naples Helsinki, Freiburg) and Asia (The Genome Institute of Singapore). We also have many collaborations within the UK including Universities of Oxford, Cambridge, Nottingham, and also with ReNeuron, a UK biotech company focusing on stem-cell therapy.
The department participates in a BSc (Intercalated) in Neuroscience and Neuropsychology pathway.
The department also runs one taught MSc course in Neuroscience. This Masters degree is offered as a one-year full-time programme and as a two-year part-time programme; it provides specialised pathways in Addiction Biology, Developmental Neurobiology, Neurodegeneration, Neuroimaging and Cognitive Neuroscience
For those wishing for supervision in doing a PhD, current vacancies can be found here.
Website:
Interests:
Cells (NSCs) and the neural progenitor cells (NPCs) that they generate is essential not only to our understanding of neurodevelopment but also in enabling us to harness the full potential of these cells for the treatment of neurodegenerative disease.
We study NSC/NPC biology in several ways.
1. We use a combination of cellular and molecular biology techniques to understand how growth in culture (in the presence of mitogens, including bFGF and EGF) influences gene expression profiles of NSCs/NPCs and hence their subsequent fate (see Price and Williams 2001; Bithell et al., 2005). The expression of key transcription factors that regulate NPC fate, and their ability to generate specific neural cell types is investigated over time in both primary cultures of NPCs and in NSC lines (immortalised and non-immortalised) isolated from different embryonic brain regions. Clonal lineage studies are carried out (see Williams et al., 1997; 1999) to determine whether all cells within a population respond similarly to growth in culture or whether the population is heterogeneous as regards gene expression profiles and developmental capabilities.
2. During forebrain development, gradients of morphogens (including SHH, BMPs, Wnts, and FGFs) direct the fate of NPCs by regulating the expression of specific sets of transcription factors. We are investigating whether different concentrations of morphogens, either alone or in combination, can be used to direct the fate of primary cultures of NPCs and NSC lines. Our goal is to be able to use this information to define culture conditions whereby NPCs/NSCs can be directed to generate a specific type of neuron or glial cell in a predictable manner.
3. We are investigating the signalling pathways that are involved in forebrain neurogenesis. During development, NPCs localised in different regions of the forebrain generate specific types of neurons. For instance, NPCs within the cortex generate mainly excitatory, glutamatergic neurons while NPCs within the ganglionic eminences generate mainly inhibitory, GABAergic neurons. These fate characteristics are maintained in primary culture when NPCs are given a neuronal differentiation signal such as Platelet-Derived Growth Factor BB (PDGF BB, see Williams et al., 1997). Using mutant and wild type chimeric PDGF receptors, together with inhibitors of particular downstream signalling pathways, we are attempting to identify which pathways are important for instructing NPCs from different regions to generate neurons.
4. We have an ongoing collaboration with Professor Noel Buckley, who will shortly join the CCBB at the Institute of Psychiatry, studying neurogenesis in the developing rodent forebrain (see Williams et al., 2004). At present we are investigating the role of the transcription factor REST in regulating gene expression and cell fate during neurogenesis and in differentiated neurons of the mouse forebrain. To do this we are generating mice carrying a floxed allele of REST (RESTfl/fl) in order to conditionally knock out this gene in the embryonic or adult brain by crossing RESTfl/fl mice with cre transgenic mice strains that will ablate the REST allele specifically in either the neuroepithelium or in differentiated forebrain neurons.
5. Other research in the laboratory involves studying the dysregulation of genes in psychiatric disorders. Here we specifically study the expression of a range of genes (both known and novel) that we have shown to be up- or down-regulated during neuronal differentiation (Bithell et al., 2003). This work is carried out in collaboration with Professor Ian Everall at the University of San Diego, USA.
We study NSC/NPC biology in several ways.
1. We use a combination of cellular and molecular biology techniques to understand how growth in culture (in the presence of mitogens, including bFGF and EGF) influences gene expression profiles of NSCs/NPCs and hence their subsequent fate (see Price and Williams 2001; Bithell et al., 2005). The expression of key transcription factors that regulate NPC fate, and their ability to generate specific neural cell types is investigated over time in both primary cultures of NPCs and in NSC lines (immortalised and non-immortalised) isolated from different embryonic brain regions. Clonal lineage studies are carried out (see Williams et al., 1997; 1999) to determine whether all cells within a population respond similarly to growth in culture or whether the population is heterogeneous as regards gene expression profiles and developmental capabilities.
2. During forebrain development, gradients of morphogens (including SHH, BMPs, Wnts, and FGFs) direct the fate of NPCs by regulating the expression of specific sets of transcription factors. We are investigating whether different concentrations of morphogens, either alone or in combination, can be used to direct the fate of primary cultures of NPCs and NSC lines. Our goal is to be able to use this information to define culture conditions whereby NPCs/NSCs can be directed to generate a specific type of neuron or glial cell in a predictable manner.
3. We are investigating the signalling pathways that are involved in forebrain neurogenesis. During development, NPCs localised in different regions of the forebrain generate specific types of neurons. For instance, NPCs within the cortex generate mainly excitatory, glutamatergic neurons while NPCs within the ganglionic eminences generate mainly inhibitory, GABAergic neurons. These fate characteristics are maintained in primary culture when NPCs are given a neuronal differentiation signal such as Platelet-Derived Growth Factor BB (PDGF BB, see Williams et al., 1997). Using mutant and wild type chimeric PDGF receptors, together with inhibitors of particular downstream signalling pathways, we are attempting to identify which pathways are important for instructing NPCs from different regions to generate neurons.
4. We have an ongoing collaboration with Professor Noel Buckley, who will shortly join the CCBB at the Institute of Psychiatry, studying neurogenesis in the developing rodent forebrain (see Williams et al., 2004). At present we are investigating the role of the transcription factor REST in regulating gene expression and cell fate during neurogenesis and in differentiated neurons of the mouse forebrain. To do this we are generating mice carrying a floxed allele of REST (RESTfl/fl) in order to conditionally knock out this gene in the embryonic or adult brain by crossing RESTfl/fl mice with cre transgenic mice strains that will ablate the REST allele specifically in either the neuroepithelium or in differentiated forebrain neurons.
5. Other research in the laboratory involves studying the dysregulation of genes in psychiatric disorders. Here we specifically study the expression of a range of genes (both known and novel) that we have shown to be up- or down-regulated during neuronal differentiation (Bithell et al., 2003). This work is carried out in collaboration with Professor Ian Everall at the University of San Diego, USA.
Tel:
020 7848 0097
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Work in our research group focuses on mechanisms of nerve cell death in Alzheimer's disease and motor neurone disease (also known as amyotrophic lateral sclerosis -ALS). We are particularly interested in axonal transport and signal transduction in the nervous system since there is evidence that these processes are disrupted in Alzheimer's disease and ALS.
Tel:
020 7848 0393
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Tau, a microtubule-associated protein implicated in the development of pathology in Alzheimers disease, progressive supranuclear palsy and related tauopathies. This laboratory is particularly interested in the phosphorylation status of tau in disease and in the protein kinases involved in pathological and physiological phosphorylation of tau.
Alpha-synuclein, a pre-synaptic protein present in Lewy bodies in the brain of people with Parkinsons disease, Dementia with Lewy bodies, multiple system atrophy and related disorders. Dr Hanger is investigating biochemical modifications and functional abnormalities in this protein and their implications for diseases in which alpha-synuclein plays a pathological role.
A wide range of techniques is used in these research projects, including protein chemistry, cell and molecular biology. In conjunction with Proteome Sciences plc, we are also using new methods in mass spectrometry to investigate post-translational modifications of disease-associated proteins.
Tel:
020 7848 0041
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Research has focused on the evolution, development, and disease of the brain using Drosophila as a model system. These neurogenetic studies have significantly contributed to the identification of evolutionary conserved genetic mechanisms underlying insect and mammalian brain development, and which led to the current view of a common origin of the bilaterian brain. More recent research significantly contributed to the discovery of a new molecular pathway regulating neural stem- and progenitor cell self-renewal, which has a major impact for understanding cancer stem cell driven brain tumorigenesis as well as to devise new therapeutic strategies in regenerative medicine. Recent interests combine research in stem cell biology and neurodegeneration, and are directed towards the identification of genes and mechanisms regulating stem/progenitor cell proliferation and neuronal specification. These include research on stem cell self-renewal, brain tumor suppression, and Parkinson's disease.
Tel:
020 7848 0786
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Transplanted neural stem cells have a unique ability to restore the behavioural and structural deficits associated with chronic neural damage. Our group is engaged in studies to try to understand the biological basis of this repair process, and to translate this understanding into new therapies for intractable neurological disorders in patients.
Tel:
020 7848 0948
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Application of human genetics to the study of neurological and psychiatric disorders; in particular the neurological disorders, Alzheimer's disease and motor neurone disease and the psychiatric disorders schizophrenia and autism.
Tel:
020 7848 0630
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Neuropharmocology, neurophysiology. Please visit http://www.kcl.ac.uk/iop/depts/neuroscience/index.aspx
Tel:
020 7848 0374
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Research has focused upon the neurobiology of Batten Disease or neuronal ceroid lipofuscinosis (NCLs). Batten disease is the collective name for a group of neurodegenerative childhood disorders that invariably prove fatal, with no effective treatment available. Together with colleagues in the US, Europe and New Zealand, we are working to discover precisely how Batten disease affects the brain.
The main thrust of this work is to study patterns of neurodegeneration in mouse and large animal models of NCL, comparing our findings with the brains of affected individuals. In this manner we can identify and follow the earliest effects of disease and discover how and why these changes subsequently develop. These studies not only provide us with important landmarks of disease progression, but also the ability to judge the efficacy of candidate therapeutic strategies.
Particular interests include: the comparative study of NCL pathogenesis; the role of neuroimmune and autoimmune responses in the NCLs and other storage disorders; the developmental neurobiology of the NCLs; assessment of therapeutic efficacy.
Other collaborative studies with colleagues in the Institute's Neurodegeneration IRG continue to explore the role of novel proteins in neurodegenerative mechanisms.
Tel:
020 7848 0286
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Memory processes, including memory formation, storage, retrieval, and extinction, are fundamental for brain function and they are affected in various psychiatric illnesses such as mental retardation, Alzheimer's disease, and post-traumatic stress disorder. Currently, the biological basis of memory processes is not sufficiently well understood to develop successful treatments for memory dysfunctions. However, the advent of sophisticated molecular techniques now allows for an advanced analysis of memory processes in experimental animals, which promises to be translated for the patients.
Tel:
020 7848 5402
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Axonal transport, mitochondria, molecular motors, neurodegeneration.
Tel:
020 7848 0086
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The main interest of Dr Modo's research lies in the restorative neurobiology following brain damage, with a particular interest in cerebral ischaemia and neurodegeneration. An interdisciplinary approach encompassing in vivo and ex vivo methods probes the functional, immunological, and histological consequences of brain damage. Our aim is to stimulate and/or supplement the potential of endogenous repair mechanisms to promote improvements in behavioural impairments. To this end, we also study the neurobiology of brain development/degeneration and its relation to neoplastic formations.
Recent research efforts are aimed to use non-invasive methods, such as neuroimaging (MRI and PET), to visualise brain damage and how restorative strategies (such as stem cell migration and integration) lead to functional improvements after insults to the brain. Especially the developments in molecular imaging currently under way promise new vistas to probe the repair of the central nervous system in vivo. These novel imaging methods will provide us with means to link anatomical, metabolic, immunological, and functional changes in damaged brains to behavioural impairment and recovery.
Tel:
020 7848 0524
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Schizophrenia is a common, yet severe, psychiatric condition, affecting nearly 1% of the world population. The symptoms that define the disorder are diverse and variably expressed, and include disorganised thought, delusions, auditory hallucinations, mood disturbances and social withdrawal. Schizophrenia typically has an onset in early adulthood, and carries enormous costs to sufferers, their families and the wider society . Anti-psychotic medication remains the principal treatment for schizophrenia, although this can produce adverse side effects and generally alleviates only certain symptoms of the disorder.
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020 7848 5409
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Our interests are focused upon the transcriptional programs that operate to regulate neuronal gene expression. During embryonic life most of our 100 billion nerve cells are born. They are derived from neural stem cells, multipotent cells that have the potential to turn into any type of nerve cell. There are hundreds if not thousands of types of nerve cell - each type differing in its shape, connectivity and chemistry. This diversity of form, or phenotype, is essential to correct formation and functioning of the nervous system. Establishment and maintenance of phenotype requires that particular sets of genes are activated whilst others are shut down. Gene activity is regulated by transcription factors - proteins that bind to specific sets of genes and act as on/off or dimmer switches and microRNAs - short RNA molecules that switch off gene expression by destabilizing mRNA or blocking its translation. To date, our knowledge of how these 'transcriptional programmes' are established in nerve cells is almost non-existent. In no case do we know the complete set of targets of any singular transcription factor. One 'switch' we use for our studies is REST, a multifunction transcription factor that represses or silences many genes in both neural, and non-neural cells and is required for normal embryogenesis and development of the heart, as well as for neural stem cell differentiation. Furthermore, the regulation of REST and its target genes play important roles in several neuropathological conditions, including the response to ischaemic or epileptic insults, Down's syndrome, Huntington's disease and in some medulloblastomas. We have used bioinformatic approaches to identify all potential REST binding sites and target genes across multiple vertebrate genomes. Using chromatin immunoprecipiatation (ChIP) combined with DNA microarrays we can identify which target genes are operated on in which cell type and furthermore, we can map the epigenetic signature around theses sites. Combined with manipulating and measuring gene expression we are building up a profile of the cofactor platforms and chromatin modifications associated with each site. The application of this combined biochemical and bioinformatics approach allows several fundamental questions to be addressed: How many REST binding sites are there across the entire genome? Which genes are operated on in which cell types? Does this change with developmental stage? How does co-factor recruitment vary across different loci? Is this the cause or effect of distinct 'epigenetic signatures'? Currently, we are applying these approaches to neural stem cells to see how the epigenetic signature changes during neuronal and glial differentiation. Is the multipotentiality of a neural stem cells reflected in its chromatin structure? How does this change as commitment and differentiation proceed? Another application of this approach is the study of transcriptional dysfunction during neurological illness. For these studies we focus on the interaction between REST and huntingtin, an interaction that is disrupted in the presence of the mutant huntingtin allele leading to decreased expression of specific genes such as BDNF, a vital survival factor for striatal neurons. This gives a genome-wide perspective on transcriptional dysfunction in Huntington's disease and can potentially identify biomarkers or therapeutic targets.
Tel:
020 7848 0784
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Notch signalling in memory and Alzheimer's disease.
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020 7848 5245
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Mutations in presenilin 1 (PS1) may account for -50% of all familial Alzheimer's disease (FAD) cases. Recently, we identified PS1 as a scaffold protein regulating the sequential phosphorylation of beta-catenin by PKA and GSK-3beta, which is required for the efficient degradation of beta-catenin by the proteasome. PS1 FAD mutations represent a loss of this function and lead to deficient beta-catenin phosphorylation and degradation, resulting in cell cycle abnormalities that are secondary to abnormal beta-catenin accumulation. This phenotype is present in the brain of transgenic mice harbouring PS1 FAD mutations and our laboratory is actively investigating its implications for the pathology of PS1-linked FAD.
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020 7848 0578
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Research over the last 5 years has firmly established that learning and memory abilities, as well as mood can be influenced by diet. Although the mechanisms by which diet modulates mental health are not well understood. One of the brain structure associated with learning and memory as well as mood is the hippocampus. Interestingly, the hippocampus is one of the two structures in the adult brain where the formation of newborn neurons (or neurogenesis) persists. The level of neurogenesis in the adult hippocampus has been linked directly to cognition and mood. Therefore modulation of adult hippocampal neurogenesis by diet emerges as a possible mechanism by which nutrition impacts on mental health. In the Thuret Lab, we are studying the mechanisms by which diet modulates adult hippoacampal neurogenesis and impact on cognition and mood. If you want to know more about The Thuret lab please visit our webpage: http://www.iop.kcl.ac.uk/departments/?locator=622&context=872
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020 7848 5405
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We are particularly interested in the relationship between tau phosphorylation, aggregation and filament formation during the development of pathology in Alzheimers diseaseand related tauopathies, and are examining the impact of protein kinase inhibitors as potential therapeutic agents for the treatment of tauopathy.
Tel:
020 7848 0087
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We use an embryonic stem (ES) differentiation model to explore NS cell formation process. To obtain the genes involved in this process, we have created a novel RNAi functional screening system, MARs (Mme I-assisted random shRNA). The obtained genes will be further investigated their biological functions in vivo. Stem cells with capabilities for self-renewal and generating a variety of tissue cells have seized people's attention. Especially, neural stem (NS) cells stand out in the crowd for their potential to treat the most intricate organ, the brain, in neurodegenerative diseases, genetic disorders, stroke, spinal injury and cancer. Progress has been made in harvesting NS cells from different sources and in transplanting NS cells to the needed regions of the central nerve system (CNS). However, the safety, effective use and limited supply of NS cells in neural repair remain as a hurdle for the therapeutic invention. The fundamental knowledge of the molecular programme directing NS cell development may bear solutions for those problems. Our project is undertaken to genome-wide screen for the genes involved in NS cell developmental process using a novel strategy. This strategy combines selective subtractive hybridisation to identify differentially expressed genes during NS cell developmental process and RNAi knockdown system to functionally screen for those genes involved in the developmental process. The understanding wholesale molecular programme responsible for NS cell formation may lead to develop drugs for NS cell survival, maintenance and proliferation.
Tel:
020 7848 5311
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