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Neurodegeneration & Clinical Trials
DESCRIPTION
Professor Clive Ballard leads the Neurodegeneration Disease Group. There remains much to understand about the nature of specific disease states (eg Alzheimer's; MS and Vascular Dementia), how disease propagates throughout the brain (eg prion proteins), how we get drugs into the brain and the effectiveness of current and novel therapies for disease. A number of people within CARD have either a specific interest in a particular disease state and/or are close to application and evaluation of novel therapies for disease. Others are actively investigating age-related and genetically determined degeneration of the retina and the mechanisms of cataract formation and their treatment.Associated research programmes
Associated staff research interests
Interests:
As the age of the population increases, dementia is becoming increasingly frequent in western countries. Already there are more than 700,000 people with dementia in the UK and the number is likely to double in the next 30 years. Our group is adopting a variety of scientific approaches to understand the basis of key symptoms in people with dementia, to determine the mechanisms underlying dementia and to develop new treatments, with a particular emphasis on non-Alzheimer’s dementia such as those related to stroke, Parkinson’s Disease and Downs Syndrome.
Tel:
020 7848 8054
Fax:
020 7848 6145
Email:
Website:
Interests:
(Head of group) Age-related degenerations of the eye: interaction of light and lasers with ocular tissues.
Tel:
020 7188 4296
Email:
Interests:
Our studies have concentrated on identifying the specific retinoic acid receptor (RAR) signalling pathways in neurite outgrowth, neuronal survival and stem/progenitor cell differentiation. The identification of these pathways allows the design of retinoids, these are small molecules which can cross the blood brain barrier. These retinoids are either agonists or antagonists and may have therapeutic potential in CNS disorders, such as Alzheimer’s disease, stroke and spinal cord injury.
Tel:
020 7848 6156
Fax:
020 7848 6816
Email:
Website:
Interests:
Neurochemistry of Alzheimer’s disease
Alzheimer’s disease (AD) affects over 500,000 people in the UK and the annual cost of care is estimated at £11 billion. The disease is characterised by regionally selective gross cerebral atrophy, senile plaques, neurofibrillary tangles together with selective neurone and synapse loss. The principal neuronal types affected used glutamate or acetylcholine as transmitter. These changes produce a characteristic clinical syndrome of progressive cognitive dysfunction and behavioural abnormalities with declining activities of daily living. Current treatments are based reducing the breakdown of acetylcholine in the synaptic cleft and they provide symptomatic benefit for a majority of patients.
The research of this group focuses on the relationship between neurochemical changes in the brains of patients with AD and their particular symptoms. Thus we have shown that, in addition to the well-known relationship between acetylcholine and cognitive decline , there is a relationship between this system and non-cognitive, behavioural changes seen in patients with AD. This then provides a scientific rationale for the clinical improvement in this domain following treatment with acetylcholinesterase inhibitors (AChEI).
We are also interested in the mechanism of action of AChEIs and a newly approved drug in the AD field, memantine (Ebixa, Lundbeck). We have argued that AChEIs work by increasing the release of glutamate that is reduced in AD as a consequence of glutamatergic cell and synapse loss . Memantine appears to have a glutamatergic mechanism of action, but one that is possibly at odds with our working hypothesis. We are keen to resolve this possible conflict.
Another area of great interest is second messenger/signalling systems that may be altered as a consequence of disturbed neurotransmission or as a primary pathological event. In collaboration with Dr Robert Williams we are investigating the status of signalling pathways involved in cell death and cell survival and using model systems to test whether any changes are a cause or consequence of AD neurochemical pathology.
Alzheimer’s disease (AD) affects over 500,000 people in the UK and the annual cost of care is estimated at £11 billion. The disease is characterised by regionally selective gross cerebral atrophy, senile plaques, neurofibrillary tangles together with selective neurone and synapse loss. The principal neuronal types affected used glutamate or acetylcholine as transmitter. These changes produce a characteristic clinical syndrome of progressive cognitive dysfunction and behavioural abnormalities with declining activities of daily living. Current treatments are based reducing the breakdown of acetylcholine in the synaptic cleft and they provide symptomatic benefit for a majority of patients.
The research of this group focuses on the relationship between neurochemical changes in the brains of patients with AD and their particular symptoms. Thus we have shown that, in addition to the well-known relationship between acetylcholine and cognitive decline , there is a relationship between this system and non-cognitive, behavioural changes seen in patients with AD. This then provides a scientific rationale for the clinical improvement in this domain following treatment with acetylcholinesterase inhibitors (AChEI).
We are also interested in the mechanism of action of AChEIs and a newly approved drug in the AD field, memantine (Ebixa, Lundbeck). We have argued that AChEIs work by increasing the release of glutamate that is reduced in AD as a consequence of glutamatergic cell and synapse loss . Memantine appears to have a glutamatergic mechanism of action, but one that is possibly at odds with our working hypothesis. We are keen to resolve this possible conflict.
Another area of great interest is second messenger/signalling systems that may be altered as a consequence of disturbed neurotransmission or as a primary pathological event. In collaboration with Dr Robert Williams we are investigating the status of signalling pathways involved in cell death and cell survival and using model systems to test whether any changes are a cause or consequence of AD neurochemical pathology.
Tel:
020 7848 6269
Fax:
020 7848 6145
Email:
Website:
Interests:
Intracellular trafficking and the membrance micro-environment of prion protein and their effects on normal physiological function and in transmissible spongiform encephalopathies.
Tel:
020 7848 6801
Email:
Website:
Interests:
The main focus of work in my research group is in identifying new targets for reducing abnormally overactive glutamate and GABA signalling in the basal ganglia in Parkinson's disease. Targets of interest include the Gi/Go coupled receptors purported to negatively regulate transmitter release. Such targets may offer an alternative route to symptom relief and neuroprotection in this debilitating disease. We are also interested in finding ways to provide protection against cell loss or to permit neuroregeneration in Parkinson's disease. We use a range of molecular, cellular and whole system approaches to address these issues.
Tel:
020 7848 6013
Fax:
020 7848 6145
Email:
Website:
CONTACTS FOR FURTHER INFORMATION
See our website for individual supervisor projects and contact details.
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