Gordon Wilcock

ORCID: 0000-0003-0163-3021
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Dementia and Cognitive Impairment Research
  • Alzheimer's disease research and treatments
  • Cholinesterase and Neurodegenerative Diseases
  • Health Systems, Economic Evaluations, Quality of Life
  • Neurological Disorders and Treatments
  • Frailty in Older Adults
  • Memory and Neural Mechanisms
  • Neurological Disease Mechanisms and Treatments
  • Functional Brain Connectivity Studies
  • Genetic Associations and Epidemiology
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Computational Drug Discovery Methods
  • Tryptophan and brain disorders
  • Cerebrovascular and genetic disorders
  • Bioinformatics and Genomic Networks
  • Schizophrenia research and treatment
  • Nerve injury and regeneration
  • Health, Environment, Cognitive Aging
  • Cerebrovascular and Carotid Artery Diseases
  • Geriatric Care and Nursing Homes
  • Chemical synthesis and alkaloids
  • Intergenerational Family Dynamics and Caregiving
  • Acute Ischemic Stroke Management
  • Folate and B Vitamins Research
  • Neuroscience and Neuropharmacology Research

University of Oxford
2014-2023

John Radcliffe Hospital
2011-2022

Science Oxford
2019

University of Bristol
2002-2017

University of Cambridge
2014-2016

University of Gothenburg
2016

University of Toronto
2016

Sunnybrook Health Science Centre
2016

National University of Singapore
2016

Oxford Fertility
2015

10.1016/0022-510x(82)90155-1 article EN Journal of the Neurological Sciences 1982-11-01

A new assessment of Activities Daily Living has been developed specifically for use with people dementia. The is a carer rated instrument consisting 20 daily-living abilities. scale 'face validity', assessing items as important by and using levels ability generated carers. It 'construct' validity demonstrated principal components analysis. 'concurrent' in that it correlates well observed task performance. good 'test–retest' reliability measured Cohen's Kappa the Mini-Mental State...

10.1093/ageing/25.2.113 article EN Age and Ageing 1996-01-01

10.1016/0022-510x(82)90045-4 article EN Journal of the Neurological Sciences 1982-12-01

Abstract: Markers of serotonin synapses in entire temporal lobe and frontal neocortex were examined for changes Alzheimer's disease by use both neurosurgical autopsy samples. Uptake [ 3 H]sero‐tonin, binding H]imipramine, content indola‐mines all significantly reduced, indicating that nerve terminals are affected. Binding H]serotonin was also whereas H]qui‐nuclidinyl benzilate, H]muscimol, H]dihydroal‐prenolol unaltered. When the samples subdivided according to age, reduction a feature only...

10.1111/j.1471-4159.1983.tb11838.x article EN Journal of Neurochemistry 1983-01-01

Multiple neurotransmitter deficits found in recent autopsy studies of patients with Alzheimer's disease may militate against the success "simple cholinergic replacement" as treatment. To study acetylcholine synthesis, we measured incorporation radiolabeled glucose into transmitter temporal-cortex specimens obtained at diagnostic craniotomy 17 young disease. Synthesis was significantly correlated cognitive impairment. These results are consistent view that deficit presynaptic system is a...

10.1056/nejm198507043130102 article EN New England Journal of Medicine 1985-07-04

Agitation is a common and distressing symptom in patients with Alzheimer's disease. Cholinesterase inhibitors improve cognitive outcomes such patients, but the benefits of these drugs for behavioral disturbances are unclear.

10.1056/nejmoa066583 article EN New England Journal of Medicine 2007-10-03

LMTM is being developed as a treatment for AD based on inhibition of tau aggregation.To examine the efficacy monotherapy in non-randomized cohort analyses modified primary outcomes an 18-month Phase III trial mild AD.Mild patients (n = 800) were randomly assigned to 100 mg twice day or 4 day. Prior unblinding, Statistical Analysis Plan was revised compare subgroup 79) versus randomized 396), and 76) add-on therapy 297), with strong control family-wise type I error.The statistically...

10.3233/jad-170560 article EN other-oa Journal of Alzheimer s Disease 2017-11-17

Interleukin-1 (IL-1) is markedly overexpressed in Alzheimer's disease. We found the IL-1A 2,2 genotype 12.9% of 232 neuropathologically confirmed disease patients and 6.6% 167 controls from four centers United Kingdom States (odds ratio, 3.0; controlled for age ApoE [apolipoprotein E] genotype). Homozygosity both allele 2 IL-1B conferred even greater risk 10.8). IL-1 genotypes may confer through overexpression IL-1-driven neurodegenerative cascades.

10.1002/1531-8249(200003)47:3<365::aid-ana13>3.0.co;2-g article EN Annals of Neurology 2000-03-01

<h3>OBJECTIVES</h3> To better define the neuropathology of vascular dementia. <h3>METHODS</h3> The neuropathological findings in 18 elderly, undemented subjects free cerebrovascular disease were compared with 19 elderly who had (many whom a "stroke") and 24 demented disease, but no other pathology to account for Cases all groups selected absence or more than very mild Alzheimer type pathology. <h3>RESULTS</h3> Microvascular brain damage form severe cribriform change associated subcortical...

10.1136/jnnp.63.6.749 article EN Journal of Neurology Neurosurgery & Psychiatry 1997-12-01

Abstract A viral aetiology has long been suspected for Alzheimer's disease (AD) but until now, techniques have not sufficiently sensitive to provide clear evidence or against the presence of any genome in AD brain. We used very highly method polymerase chain reaction look herpes simplex virus type 1 (HSV1) DNA, specifically thymidine kinase (TK) gene, autopsy brain specimens. DNA samples from HSV‐infected and uninfected Vero cells examined concurrently standard “HSV‐positive” “HSV‐negative”...

10.1002/jmv.1890330403 article EN Journal of Medical Virology 1991-04-01

Background:The metabolic syndrome is a risk factor for cardiovascular diseases, which have been linked to Alzheimer disease.However, link between disease and the has not yet established. Objective:To investigate relationship disease.Design, Setting, Participants: Case-control study of 50 consecutive patients diagnosed with probable from Memory Disorders Clinics, Launceston, Australia, Bristol, England, 75 cognitively normal controls. Main Outcome Measures:The odds ratio as defined by...

10.1001/archneur.64.1.93 article EN Archives of Neurology 2007-01-01

To assess the safety of galantamine in subjects with mild cognitive impairment (MCI), ability to benefit cognition and global functioning MCI, delay conversion dementia.In two studies, 2,048 subjects, 990 Study 1 1,058 2, a Clinical Dementia Rating (CDR) = 0.5, CDR memory score > or =0.5, without dementia were randomized double-blind (16-24 mg/day) placebo for 24 months. Primary efficacy endpoint at month was number (%) who converted from MCI (CDR 1.0).There no differences between 24-month...

10.1212/01.wnl.0000303815.69777.26 article EN Neurology 2008-03-06

Article AbstractObjective: Long­standing evidence indicates that Alzheimer's disease patients with behavioral symptoms have a worse prognosis and more rapid progression. The current retrospective analysis evaluated the efficacy safety of memantine in subpopulation exhibiting agitation/aggression or psychosis at baseline. Method: A pooled was conducted people from 3 large 6-month, randomized studies moderately severe to disease. effect placebo on these specific using Neuropsychiatric...

10.4088/jcp.v69n0302 article EN The Journal of Clinical Psychiatry 2008-03-15
Coming Soon ...