Prof Gordon Wilcock
| Research Area: | Behavioural Science |
|---|---|
| Keywords: | dementia, Alzheimer's Disease, clinical trials, ageing and biomarkers |
| Web Links: |
Gordon Wilcock has been involved in Alzheimer's disease (AD) research since the late seventies and was also the founder chairman of the Alzheimer's Disease Society (now the Alzheimer's Society).
His early research explored the neuropathology of Alzheimer's disease and its relation to the clinical presentation, and also the underlying neurochemical pathology which contributed to the development of the currently available drugs for AD. He established an internationally respected research programme in Bristol, which spanned the spectrum from molecular technology and pathology in the laboratory at one end, to the patient and carer at the other. The latter included the earliest work on one of the drugs now licensed for AD, and also evaluation of the others. His work in Oxford, where is a Professor of Clinical Geratology, is concentrating on translating basic scientific knowledge about Alzheimer's disease into the clinical setting, especially in relation to new treatments and biomarkers for diagnosis, including imaging. He has collaborative research projects with a number of other centres, in the United Kingdom and abroad.
His clinical interests in Oxford are centred on the dementias, both in a local service context and also nationally with the Government’s National Dementia Strategy.
| Name | Department | Institution | Country |
|---|---|---|---|
| Zsuzsanna Nagy | University of Birmingham | UK | |
| J Zajicek | Peninsula Medical School | UK | |
| R Jones | University of Bath | UK | |
| R Foster | University of Oxford | UK | |
| Irene Tracey | FMRIB centre, University of Oxford | UK | |
| L Scheneider | University of Southern California | USA | |
| Bruno Vellas | University of Toulouse | France |
2010. Retrospective evaluation of revised criteria for the diagnosis of Alzheimer's disease using a cohort with post-mortem diagnosis. Int J Geriatr Psychiatry, 25 (10), pp. 988-997. Read abstract | Read more
The criteria currently used to diagnose Alzheimer's disease (AD) require the presence of dementia, i.e. cognitive impairment sufficient to affect normal social and/or occupational function. Dubois et al. (Dubois et al., 2007) have recently proposed a set of revised criteria that may aid the diagnosis of the earlier stages of AD, and do not require the presence of dementia. We aimed to evaluate the new predementia-AD criteria through their retrospective application to the OPTIMA cohort with post-mortem (PM) confirmed diagnoses. Hide abstract
2010. Bapineuzumab in Alzheimer's disease: where now? Lancet Neurol, 9 (2), pp. 134-136. | Read more
2009. Predicting the time of conversion to MCI in the elderly: role of verbal expression and learning. Neurology, 73 (18), pp. 1436-1442. Read abstract | Read more
Increasing awareness that minimal or mild cognitive impairment (MCI) in the elderly may be a precursor of dementia has led to an increase in the number of people attending memory clinics. We aimed to develop a way of predicting the period of time before cognitive impairment occurs in community-dwelling elderly. The method is illustrated by the use of simple tests of different cognitive domains. Hide abstract
2009. Cholinesterase inhibitors may increase phosphorylated tau in Alzheimer's disease. J Neurol, 256 (5), pp. 717-720. Read abstract | Read more
Cholinesterase inhibitors (ChEIs) are widely used for the symptomatic treatment of Alzheimer's disease (AD). In vitro and in animal studies, ChEIs have been shown to influence the processing of Abeta and the phosphorylation of tau, proteins that are the principal constituents of the plaques and neurofibrillary tangles, respectively, in AD brain. However, little is known about the effects of these drugs on Abeta and tau pathology in AD. Using avidin-biotin immunohistochemistry and computer-assisted image analysis, we compared Abeta and tau loads in the frontal and temporal cortices of 72 brains from matched cohorts of AD patients who had or had not received ChEIs. Patients treated with ChEIs had accumulated significantly more phospho-tau in their cerebral cortex than had untreated patients (P = 0.004). Abeta accumulation was reduced but not significantly. These data raise the possibility that increased tau phosphorylation may influence long-term clinical responsiveness to ChEIs. Hide abstract
2008. Efficacy and safety of tarenflurbil in mild to moderate Alzheimer's disease: a randomised phase II trial. Lancet Neurol, 7 (6), pp. 483-493. Read abstract | Read more
The amyloid-beta peptide Abeta(42) has been implicated in the pathogenesis of Alzheimer's disease (AD). We aimed to test the effects of tarenflurbil, a selective Abeta(42)-lowering agent (SALA), on cognition and function in patients with mild to moderate AD. Hide abstract
2008. Endpoints for trials in Alzheimer's disease: a European task force consensus. Lancet Neurol, 7 (5), pp. 436-450. Read abstract | Read more
Harmful consequences in health status caused by disease are referred to as outcomes, and in clinical studies the measures of these outcomes are called endpoints. A major challenge when deciding on endpoints is to represent the outcomes of interest accurately, and the accuracy of such representation is assessed through validation. Complex diseases like Alzheimer's disease have many different and interdependent outcomes. We present a consensus for endpoints to be used in clinical trials in Alzheimer's disease, agreed by a European task force under the auspices of the European Alzheimer Disease Consortium. We suggest suitable endpoints for primary and secondary prevention trials, for symptomatic and disease-modifying trials in very early, mild, and moderate Alzheimer's disease, and for trials in severe Alzheimer's disease. A clear and consensual definition of endpoints is crucial for the success of further clinical trials in the field and will allow comparison of data across studies. Hide abstract
2008. Memantine for agitation/aggression and psychosis in moderately severe to severe Alzheimer's disease: a pooled analysis of 3 studies. J Clin Psychiatry, 69 (3), pp. 341-348. Read abstract
Long-standing evidence indicates that Alzheimer's disease patients with behavioral symptoms have a worse prognosis and a more rapid disease progression. The current retrospective analysis evaluated the efficacy and safety of memantine in a subpopulation of patients with Alzheimer's disease exhibiting behavioral symptoms of agitation/aggression or psychosis at baseline. Hide abstract
2007. Is inhibition of the renin-angiotensin system a new treatment option for Alzheimer's disease? Lancet Neurol, 6 (4), pp. 373-378. Read abstract | Read more
Findings from longitudinal and cross-sectional studies suggest an association between high blood pressure and dementia, and in turn the use of antihypertensives has been suggested to reduce incidence of dementia. Alzheimer's disease, the most common cause of dementia, is characterised in part by the deposition of amyloid beta protein (Abeta) in the brain. Reduction of Abeta load is now a major therapeutic strategy. In recent years the renin-angiotensin system, already of recognised importance in the pathogenesis of hypertension, has become a source of interest in the pathogenesis of Alzheimer's disease. This review explores molecular, genetic, and clinical studies that might help explain the relation between the renin-angiotensin system, hypertension, and Alzheimer's disease and whether treatment with angiotensin converting enzyme (ACE) inhibitors and similar treatment strategies have a part to play in the management of the disease. Hide abstract
2007. Disease-modifying trials in Alzheimer's disease: a European task force consensus. Lancet Neurol, 6 (1), pp. 56-62. Read abstract | Read more
After symptomatic treatments, the new target for therapeutic approaches in Alzheimer's disease is the development of disease-modifying drugs. The concept of disease modification in Alzheimer's disease is controversial and the design of these trials raises many questions. Which populations should be studied? For how long? With which principal and secondary endpoints? Are surrogate markers available? Here, we present a European consensus on disease-modifying trials in Alzheimer's disease, agreed under the auspices of the European Alzheimer's Disease Consortium and based on the European perspective of the concept of disease modification, study designs, the role for biomarkers, risk benefit, and pharmacoeconomic issues. Hide abstract
2007. The metabolic syndrome and Alzheimer disease. Arch Neurol, 64 (1), pp. 93-96. Read abstract | Read more
The metabolic syndrome is a risk factor for cardiovascular diseases, which have been linked to Alzheimer disease. However, a link between Alzheimer disease and the metabolic syndrome has not yet been established. Hide abstract
