Clive Holmes

ORCID: 0000-0003-1999-6912
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Dementia and Cognitive Impairment Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Tryptophan and brain disorders
  • Genetic Associations and Epidemiology
  • Bioinformatics and Genomic Networks
  • Neurological Disease Mechanisms and Treatments
  • Health Systems, Economic Evaluations, Quality of Life
  • Cholinesterase and Neurodegenerative Diseases
  • Geology and Paleoclimatology Research
  • Computational Drug Discovery Methods
  • Genomics and Rare Diseases
  • Schizophrenia research and treatment
  • Geological formations and processes
  • Folate and B Vitamins Research
  • Neurological Disorders and Treatments
  • Rheumatoid Arthritis Research and Therapies
  • Nutrition, Genetics, and Disease
  • Medicinal Plant Extracts Effects
  • Parkinson's Disease Mechanisms and Treatments
  • Stress Responses and Cortisol
  • Treatment of Major Depression
  • Diet and metabolism studies
  • Pharmaceutical Practices and Patient Outcomes
  • Intensive Care Unit Cognitive Disorders

University of Southampton
2015-2024

Moorgreen Hospital
2014-2024

Southern Health NHS Foundation Trust
2013-2024

Health Foundation
2013-2024

Oxford University Hospitals NHS Trust
2024

Genomics (United Kingdom)
2020

University of Pennsylvania
2017-2020

Keele University
2019

Southampton General Hospital
2005-2019

The University of Texas Health Science Center at San Antonio
2018

10.1038/ng.440 article EN Nature Genetics 2009-09-06

Objective: To prospectively validate the Montreal Cognitive Assessment (MoCA) in a UK memory clinic. Method: We administered MoCA and Mini-Mental State Examination (MMSE) to 32 subjects fulfilling diagnostic criteria for dementia, 23 mild cognitive impairment (MCI), 12 clinic comparison subjects, at baseline then 6-month follow-up. Clinical diagnoses dementia MCI were made according ICD-10 Petersen criteria. The sensitivity specificity of both measures assessed detection dementia. Results:...

10.1177/070674370705200508 article EN The Canadian Journal of Psychiatry 2007-05-01

Background Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. Recent large genome-wide association studies (GWAS) identified first strongly supported LOAD susceptibility genes since discovery involvement APOE in early 1990s. We have now exploited these GWAS datasets to uncover key pathophysiological processes. Methodology applied a recently developed tool for mining data biologically meaningful information dataset. The principal findings were then tested an independent...

10.1371/journal.pone.0013950 article EN cc-by PLoS ONE 2010-11-15

The identification of subjects at high risk for Alzheimer's disease is important prognosis and early intervention. We investigated the polygenic architecture accuracy prediction models, including excluding component in model. This study used genotype data from powerful dataset comprising 17 008 cases 37 154 controls obtained International Genomics Project (IGAP). Polygenic score analysis tested whether alleles identified to associate with one sample set were significantly enriched relative...

10.1093/brain/awv268 article EN Brain 2015-10-21

Periodontitis is common in the elderly and may become more Alzheimer's disease because of a reduced ability to take care oral hygiene as progresses. Elevated antibodies periodontal bacteria are associated with an increased systemic pro-inflammatory state. Elsewhere raised serum cytokines have been rate cognitive decline disease. We hypothesized that periodontitis would be dementia severity rapid aimed determine if both decline, pro inflammatory In six month observational cohort study 60...

10.1371/journal.pone.0151081 article EN cc-by PLoS ONE 2016-03-10

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

A major feature of Alzheimer's disease is the accumulation amyloid-β peptide (Aβ) in brain both form plaques cerebral cortex and blood vessel as amyloid angiopathy (CAA). Experimental models human clinical trials have shown that Aβ can be reversed by immunotherapy. In this study, we hypothesized solubilized antibodies generated immunization drains via perivascular pathway, detectable an increase cerebrovascular Aβ. We performed a follow up study patients immunized against Aβ42....

10.1093/brain/awn261 article EN Brain 2008-10-25

In vivo imaging of brain β-amyloid, a hallmark Alzheimer disease, may assist in the clinical assessment suspected disease. To determine sensitivity and specificity positron emission tomography with flutemetamol injection labeled radioactive fluorine 18 to detect β-amyloid using neuropathologically determined neuritic plaque levels as standard truth. Open-label multicenter study that took place at dementia clinics, memory centers, hospice centers United States England from June 22, 2010,...

10.1001/jamaneurol.2014.4144 article EN JAMA Neurology 2015-01-26
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