A5036174826- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- Functional Brain Connectivity Studies
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disease Mechanisms and Treatments
- Advanced Neuroimaging Techniques and Applications
- EEG and Brain-Computer Interfaces
- S100 Proteins and Annexins
- Neurological Disorders and Treatments
- Diabetes Treatment and Management
- Advanced MRI Techniques and Applications
- Long-Term Effects of COVID-19
- Tryptophan and brain disorders
- Medical Imaging Techniques and Applications
- Mitochondrial Function and Pathology
- Cancer-related cognitive impairment studies
- Diet and metabolism studies
- Health, Environment, Cognitive Aging
- Parkinson's Disease Mechanisms and Treatments
- Optical Imaging and Spectroscopy Techniques
- Traumatic Brain Injury and Neurovascular Disturbances
- Cerebrovascular and Carotid Artery Diseases
- COVID-19 and Mental Health
- Traumatic Brain Injury Research
- Neuroscience and Neural Engineering
Imperial College London
2016-2025
Cardiff University
2015-2025
Edison (Italy)
2019-2024
Forschungszentrum Jülich
2024
University Hospital Cologne
2024
University of Cologne
2024
University of Brescia
2024
Amyloidosis Foundation
2023
Hammersmith Hospital
2013-2022
Imperial College Healthcare NHS Trust
2011-2021
<b>Objective: </b> To investigate the association between brain amyloid load in Alzheimer disease (AD) measured by [11C]PIB-PET, regional cerebral glucose metabolism (rCMRGlc) [18F]FDG-PET, and cognition. <b>Methods: Nineteen subjects with AD 14 controls had [11C]PIB-PET underwent a battery of psychometric tests. Twelve those eight [18F]FDG-PET. Parametric images [11C]PIB binding rCMRGlc were interrogated region-of-interest atlas statistical parametric mapping. correlated scores on...
<b>Background:</b> Patients with amnestic mild cognitive impairment (MCI) represent an important clinical group as they are at increased risk of developing Alzheimer disease (AD). <sup>11</sup>C-PIB PET is in vivo marker brain amyloid load. <b>Objective:</b> To assess the rates conversion MCI to AD during a 3-year follow-up period and compare levels deposition between converters nonconverters. <b>Methods:</b> Thirty-one subjects baseline PET, MRI, neuropsychometry have been clinically...
Neuropathological studies have reported varying amounts of amyloid pathology in dementia with Lewy bodies (DLB) and Parkinson's disease (PDD). [11C]PIB positron emission tomography (PET) is a marker brain deposition. The aim this study was to quantify vivo load DLB PDD compared control subjects (PD) without dementia.13 DLB, 12 PDD, 10 PD 41 age matched controls (55-82 years) were recruited. Each subject underwent clinical evaluation, neuropsychological assessment, T1 T2 MRI, PET. estimated...
Amyloid-β deposition, neuroinflammation and tau tangle formation all play a significant role in Alzheimer's disease. We hypothesized that there is microglial activation early on disease trajectory, where the initial phase, microglia may be trying to repair damage, while later these could ineffective produce proinflammatory cytokines leading progressive neuronal damage. In this longitudinal study, we have evaluated temporal profile of its relationship between fibrillar amyloid load at...
Activated microglia may play a role in the pathogenesis of Alzheimer disease (AD) as they cluster around beta-amyloid (Abeta) plaques. They are, therefore, potential therapeutic target both AD and its prodrome amnestic mild cognitive impairment (MCI).To characterize vivo with (11)C-(R)-PK11195 (11)C-PIB PET distribution microglial activation amyloid deposition patients MCI.Fourteen subjects MCI had psychometric tests.Seven out 14 (50%) increased cortical retention (p < 0.001) while 5 13...
Alzheimer's disease is characterized by the histopathological presence of amyloid-β plaques and tau-containing neurofibrillary tangles. Microglial activation also a recognized pathological component. The relationship between microglial protein aggregation still debated. We investigated amyloid plaques, tau tangles activated microglia using PET imaging. Fifty-one subjects (19 healthy controls, 16 mild cognitive impairment subjects) participated in study. All had neuropsychometric testing,...
Abstract Background Alzheimer's disease (AD) and Parkinson's (PD) are the two common neurodegenerative diseases characterized by progressive neuronal dysfunction in presence of pathological microglial activation. Methods 10 AD, mild cognitive impairment (MCI), 11 PD dementia (PDD), 16 controls underwent magnetic resonance imaging, [11C](R)PK11195 (1‐[2‐chlorophenyl]‐N‐methyl‐N‐[1‐methyl‐propyl]‐3‐isoquinoline carboxamide), [11C]PIB (11C‐Pittsburgh compound B), [18F]FDG‐PET...
See Kreisl (doi:10.1093/awx151) for a scientific commentary on this article.Subjects with mild cognitive impairment associated cortical amyloid-β have greatly increased risk of progressing to Alzheimer's disease. We hypothesized that neuroinflammation occurs early in disease and would be present most amyloid-positive cases. 11C-Pittsburgh compound B 11C-(R)-PK11195 positron emission tomography was used determine the amyloid load detect extent (microglial activation) 42 Twelve age-matched...
Liraglutide is a glucagon-like peptide-1 (GLP-1) analogue currently approved for type 2 diabetes and obesity. Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity cerebral glucose uptake, increasing the proliferation neuronal progenitor cells. The primary objective study to evaluate change metabolic rate after 12 months treatment with participants compared those...
Abstract To determine the relationship between cerebral amyloid plaque load and rates of atrophy in Alzheimer's disease. 11 C‐PIB( C‐6‐OH benzothiazole)PET (positron emission tomography) findings were correlated with volumetric magnetic resonance imaging (MRI) measurements nine subjects mild to moderate AD. Analysis revealed a positive correlation whole brain (p = 0.019) regional C‐PIB uptake. This provides support for central role deposition pathogenesis Ann Neurol 2006;60:145–147
Amyloid PET tracers have been developed for in vivo detection of brain fibrillar amyloid deposition Alzheimer's disease (AD). To serve as an early biomarker AD the need to be analysed multicentre clinical studies.In this study 238 [(11)C]Pittsburgh compound-B (PIB) datasets from five different European centres were pooled. Of these datasets, 18 excluded, leaving [(11)C]PIB 97 patients with clinically diagnosed (mean age 69 ± 8 years), 72 mild cognitive impairment (MCI; mean 67.5 years) and...
<h3>Objective:</h3> To image β-amyloid (Aβ) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether axonal and Aβ are correlated, compare the spatial distribution to Alzheimer disease (AD). <h3>Methods:</h3> Patients 11 months 17 years after moderate–severe TBI underwent <sup>11</sup>C-Pittsburgh compound B (<sup>11</sup>C-PiB)-PET, structural diffusion MRI, neuropsychological examination. Healthy aged controls patients with AD PET MRI. Binding potential...