A5056046668- Alzheimer's disease research and treatments
- Neurological Disease Mechanisms and Treatments
- Child and Adolescent Psychosocial and Emotional Development
- Dementia and Cognitive Impairment Research
- Neurological Disorders and Treatments
- Infection Control and Ventilation
- Neuroinflammation and Neurodegeneration Mechanisms
- COVID-19 and healthcare impacts
- Obesity, Physical Activity, Diet
- Child and Adolescent Health
- COVID-19 epidemiological studies
- Traumatic Brain Injury and Neurovascular Disturbances
- Cholinesterase and Neurodegenerative Diseases
- Mental Health Research Topics
- Blood Pressure and Hypertension Studies
- Disaster Response and Management
- Obesity and Health Practices
- Cerebral Palsy and Movement Disorders
- Genetics, Aging, and Longevity in Model Organisms
- Cerebrovascular and genetic disorders
- Coronary Artery Anomalies
- Cardiovascular Health and Disease Prevention
- Computational Drug Discovery Methods
- Digital Mental Health Interventions
- Meta-analysis and systematic reviews
University of Bristol
2014-2025
UK Health Security Agency
2021-2023
MRC Epidemiology Unit
2021-2023
Dementia UK
2008-2010
Frenchay Hospital
2007-2010
McGill University
2005
Terry Fox Research Institute
2005
University of North Carolina at Chapel Hill
1970
Little is known about the contributors and physiological responses to white matter hypoperfusion in human brain. We previously showed ratio of myelin-associated glycoprotein proteolipid protein 1 post-mortem brain tissue correlates with degree ante-mortem ischaemia. In age-matched cohorts Alzheimer's disease (n = 49), vascular dementia 17) control brains 33) from South West Dementia Brain Bank (Bristol), we have now examined relationship between several other proteins involved regulating...
Abstract The earliest decline in cerebral perfusion Alzheimer's disease (AD) is the medial parietal cortex (precuneus). We have analyzed precuneus post‐mortem tissue from 70 AD and 37 control brains to explore pathophysiology of hypoperfusion: contribution arteriolosclerotic small vessel (SVD) amyloid angiopathy (CAA), vasoconstrictors endothelin‐1 (EDN1) angiotensin II (Ang II), association with Aβ. myelin‐associated glycoprotein:proteolipid protein‐1 ratio (MAG:PLP1) was used as an...
Vascular dysfunction and lowered cerebral blood flow are thought to contribute the development progression of Alzheimer's disease (AD). Endothelin-1 (ET-1) is a potent vasoconstrictor, production which mainly catalyzed by endothelin-converting enzymes (ECEs). We previously showed t hat ECE-2 upregulated amyloid-β (Aβ), its expression elevated in AD postmortem brain tissue. have now investigated whether there concomitant increase ET-1. studied temporal cortex from 20 cases sporadic matched...
Alzheimer's disease (AD) patients have reduced cerebral blood flow. This precedes dementia and may contribute to its progression. In mice that overexpress amyloid-β protein precursor, flow declines before the development of plaques or
Public health attempts to prevent obesity in children and young people should aim minimize inequalities. Two Cochrane reviews examining interventions aiming childhood found that promoting (only) physical activity have a small beneficial effect on BMI for aged 5-18 years, as do alongside healthy eating 5-11 year olds. We examined whether the effectiveness of included these differed according eight factors associated with inequity: place, race/ethnicity, occupation, gender/sex, religion,...
J. C. Palmer, P. G. Kehoe and S. Love (2010) Neuropathology Applied Neurobiology36, 487–497Endothelin-converting enzyme-1 in Alzheimer's disease vascular dementia Aims: (AD) is believed to be caused by the accumulation of amyloid beta (Aβ) peptide within brain. Endothelin-converting 2 (ECE-1 ECE-2) are expressed endothelial cells neurones, respectively, both cleave 'big endothelin' produce vasoconstrictor endothelin-1 (ET-1). ECE-1 ECE-2 also degrade Aβ. AD patients have regionally reduced...
Studies in model organisms have demonstrated that components of insulin and insulin-like signaling pathways are involved the regulation lifespan but relevance those findings to humans has remained obscure. Here we provide evidence suggesting variants gene encoding insulin-degrading enzyme (IDE) may be influencing human lifespan. We employed a variety models diverse samples reproducibly indicate relative change IDE genotype frequency across age spectrum as well allow detection association...
Abstract Background Public health attempts to prevent obesity in children and young people should aim minimize inequalities. We aimed assess whether there were differences the effectiveness of interventions included two Cochrane reviews according eight PROGRESS inequity factors. Methods collected data on change BMI (standardized or unstandardized), subgrouped by baseline measures factors, for intervention control groups, from trial authors. calculated effect per subgroup (mean difference),...
Cerebral blood flow is reduced in Alzheimer’s disease (AD), which associated with mid-life hypertension. In people increased cerebral vascular resistance due to vertebral artery or posterior communicating hypoplasia, there evidence that hypertension develops as a protective mechanism maintain perfusion. AD, amyloid-β (Aβ) accumulation may similarly raise by upregulation of the endothelin system. The level endothelin-1 brain tissue correlates positively Aβ load and negatively markers...
Mid-life hypertension and cerebral hypoperfusion may be preclinical abnormalities in people who later develop Alzheimer’s disease. Although accumulation of amyloid-beta (Aβ) is characteristic disease associated with upregulation the vasoconstrictor peptide endothelin-1 within brain, it unclear how this affects systemic arterial pressure. We have investigated whether infusion Aβ 40 into ventricular cerebrospinal fluid modulates blood pressure Dahl salt-sensitive rat. The rat develops if given...
Human T cell leukemia virus (HTLV) is the causative agent of adult (ATL), an aggressive and fatal CD4+ lymphocytes in which interferon regulatory factor-4 (IRF-4) becomes constitutively expressed, concomitant with major alterations host gene expression. When expressed uninfected lymphocytes, IRF-4 caused reduced expression critical DNA repair genes, including Rad51, XRCC1, Ung1, RPA, proliferative nuclear antigen (PCNA), a transcriptional phenotype striking similarities to profile observed...