A5004149008- Alzheimer's disease research and treatments
- Multiple Sclerosis Research Studies
- Dementia and Cognitive Impairment Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Memory and Neural Mechanisms
- Neuroscience and Neuropharmacology Research
- Neurological Disease Mechanisms and Treatments
- Peripheral Neuropathies and Disorders
- Cerebrovascular and genetic disorders
- Advanced Neuroimaging Techniques and Applications
- Cholinesterase and Neurodegenerative Diseases
- Neurological Disorders and Treatments
- Cerebrovascular and Carotid Artery Diseases
- Pituitary Gland Disorders and Treatments
- Herpesvirus Infections and Treatments
- Acute Ischemic Stroke Management
- Neurological diseases and metabolism
- Prion Diseases and Protein Misfolding
- Functional Brain Connectivity Studies
- Hemispheric Asymmetry in Neuroscience
- Glioma Diagnosis and Treatment
- Mitochondrial Function and Pathology
- Neurogenesis and neuroplasticity mechanisms
- Olfactory and Sensory Function Studies
- Amyotrophic Lateral Sclerosis Research
University of Oxford
2016-2025
John Radcliffe Hospital
2013-2024
Science Oxford
1986-2023
National and Kapodistrian University of Athens
2021
Oxford University Hospitals NHS Trust
2003-2019
St George's, University of London
2011-2019
St George’s University Hospitals NHS Foundation Trust
2011-2019
Thomas Jefferson University Hospital
2019
International Collaboration On Repair Discoveries
2016
Cardiff University
2016
One of the histological hallmarks early multiple sclerosis lesions is primary demyelination, with myelin destruction and relative sparing axons. On other hand, it widely accepted that axonal loss occurs in, responsible for, permanent disability characterizing later chronic progressive stage disease. In this study, we have used an antibody against amyloid precursor protein, known to be a sensitive marker damage in number contexts, immunocytochemical experiments on paraffin embedded varying...
The numbers and distribution of the neurofibrillary tangles neuritic plaques have been determined in several areas neocortex brains affected by various degrees severity Alzheimer disease. homotypical cortex "association" temporal, parietal, frontal lobes are severely involved, whereas motor, somatic sensory, primary visual virtually unaffected. mainly supra- infragranular layers, particularly layers III V. In all except area 18 occipital lobe, there approximately twice as many layer V III....
OBJECTIVE The term classical pituitary apoplexy describes a clinical syndrome characterized by sudden headache, vomiting, visual impairment and meningismus caused the rapid enlargement of adenoma usually due to haemorrhagic infarction tumour. Most published reports looking at features management have not differentiated between patients with subclinical apoplexy, latter diagnosed surgery. Furthermore, little is reported on outcome, in particular endocrinological, role radiotherapy. purpose...
Abstract Multiple sclerosis is still regarded primarily as a disease of the white matter. However, recent evidence suggests that there may be significant involvement gray Here, we have used magnetic resonance imaging and spectroscopy in vivo histopathology postmortem to estimate thalamic neuronal loss patients with multiple sclerosis. Our results show can substantial (30–35% reduction). We conclude neurodegenerative pathology make major contribution genesis symptoms
We have developed a novel real-time quaking-induced conversion RT-QuIC-based assay to detect alpha-synuclein aggregation in brain and cerebrospinal fluid from dementia with Lewy bodies Parkinson's disease patients. This can Dementia sensitivities of 92% 95%, respectively, an overall specificity 100% when compared Alzheimer control fluid. Patients neuropathologically confirmed tauopathies (progressive supranuclear palsy; corticobasal degeneration) gave negative results. These results suggest...
McARDLE'S syndrome,1 an inborn error of metabolism caused by a lack glycogen phosphorylase activity in skeletal muscle, is recessive condition some rarity.2 Nevertheless, it poses constant problem the differential diagnosis all forms muscular disorder. Patients usually present with this after long history inability to sustain exercise; suggested demonstration that ischemic exercise (the forearm-exercise test2) fails generate lactic acid, and confirmed open-muscle biopsy histochemical excess...
<b>Background: </b> Recent pathologic investigations have shown that neocortical lesions are frequent in multiple sclerosis (MS). Structural MRI has atrophy occurs early and can be substantial, but the specific substrate for this not been defined quantitatively. <b>Objective: To investigate cortical thickness as well neuronal, glial, synaptic densities MS. <b>Methods: We studied brain samples from 22 patients with MS 17 control subjects. Neocortical were assessed on sections stained myelin...
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...
Diffusion imaging of post mortem brains has great potential both as a reference for brain specimens that undergo sectioning, and link between in vivo diffusion studies "gold standard" histology/dissection. While there is relatively mature literature on animals, human have proven more challenging due to their incompatibility with high-performance scanners. This study presents method whole, using clinical 3-Tesla scanner 3D segmented EPI spin-echo sequence. Results eleven at 0.94 × mm...
There are no generally accepted protocols for post-mortem assessment in cases of suspected vascular cognitive impairment. Neuropathologists from seven UK centres have collaborated the development a set impairment neuropathology guidelines (VCING), representing validated consensus approach to and scoring cerebrovascular disease relation The had three stages: (i) agreement on sampling protocol criteria, through series Delphi method surveys; (ii) determination inter-rater reliability each type...
We assessed axonal loss in the normal appearing white matter of corpus callosum postmortem brains patients with multiple sclerosis, using quantitative measures both density and atrophy. The calculated total number axons was reduced significantly (mean ± SD, 5.4 × 107 3.1 107) compared controls (11.6 2.2 107, p = 0.001) a reduction (median, 34%; range, 16–56%; 0.004) area SD: 584 170 mm2; controls, 871 163 0.004). These results confirm substantial demonstrate that volume are necessary to...
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.
<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...
Tissues from 13 exceptionally early cases of multiple sclerosis were studied to identify and characterize the primary demyelinating lesion, using a variety histological immunocytochemical methods. Multifactorial cluster analysis identified five significantly distinct lesion groups, which showed progression simple microglial lesions, predominating in tissues earliest cases, complex hypercellular fully demyelinated plaques, chiefly associated with intermediate duration. Quiescent lesions...
Axonal damage is found in both acute and chronic lesions of multiple sclerosis. Direct axon counting post-mortem tissue has suggested that smaller axons might have a greater susceptibility to damage, but methodological limitations precluded unequivocal interpretation. However, as neuronal axonal sizes are linked changes would be expected with retrograde or transsynaptic degeneration following injury, we hypothesized an alternative strategy for studying this phenomenon define...