Publications
230 results found
Femminella G, Ninan S, Varley J, et al., 2014, Influence of microglial activation on hippocampal atrophy in Alzheimer's and Parkinson’s disease dementia, Alzheimer's and Dementia, Vol: 10, Pages: P830-P830, ISSN: 1552-5260
Pasqualetti G, Harris R, Rinne J, et al., 2014, Does cerebral glucose metabolism and blood flow dissociate in early stages of Alzheimer's disease?, Alzheimer's and Dementia, Vol: 10, Pages: P536-P536, ISSN: 1552-5260
Femminella GD, Edison P, 2014, Evaluation of neuroprotective effect of glucagon-like peptide 1 analogs using neuroimaging, ALZHEIMERS & DEMENTIA, Vol: 10, Pages: S55-S61, ISSN: 1552-5260
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- Citations: 36
Edison P, 2014, 3. Influence of microglial activation on neuronal function in Alzheimer's and Parkinson's disease dementia, Annual Meeting of American Academy of Neurology
Matthews PM, Edison P, Geraghty OC, et al., 2014, The emerging agenda of stratified medicine in neurology, NATURE REVIEWS NEUROLOGY, Vol: 10, Pages: 15-26, ISSN: 1759-4758
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- Citations: 23
McMillan A, Paniccia L, Glasser M, et al., 2013, THE IMPACT OF CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP) THERAPY ON COGNITIVE FUNCTION IN OLDER PEOPLE WITH SLEEP DISORDERED BREATHING (SDB) AND CO MORBIDITY, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A4-A4, ISSN: 0040-6376
Ikoma Y, Edison P, Ramlackhansingh A, et al., 2013, Reference region automatic extraction in dynamic [<SUP>11</SUP>C]PIB, JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Vol: 33, Pages: 1725-1731, ISSN: 0271-678X
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- Citations: 19
Edison P, Carter SF, Rinne JO, et al., 2013, Comparison of MRI based and PET template based approaches in the quantitative analysis of amyloid imaging with PIB-PET, NEUROIMAGE, Vol: 70, Pages: 423-433, ISSN: 1053-8119
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- Citations: 44
Edison P, Fan Z, Aman Y, et al., 2013, Influence of Neuroinflammation on Neuronal Function in Neurodegenerative Diseases: An 11C-(R)-PK11195 and 18F-FDG PET Study, 65th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Edison P, Fan Z, Aman Y, et al., 2013, Influence of Neuroinflammation on Neuronal Function in Neurodegenerative Diseases: An 11C-(R)-PK11195 and 18F-FDG PET Study, 65th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Edison P, Ahmed I, Fan Z, et al., 2013, Microglia, Amyloid, and Glucose Metabolism in Parkinson’sDisease with and without Dementia, Neuropsychopharmacology
[11C](R)PK11195-PET measures upregulation of translocator protein, which is associated with microglial activation, [11C]PIB-PET is amarker of amyloid, while [18F]FDG-PET measures cerebral glucose metabolism (rCMRGlc). We hypothesize that microglial activation isan early event in the Parkinson’s disease (PD) spectrum and is independent of the amyloid pathology. The aim of this study is to evaluatein vivo the relationship between microglial activation, amyloid deposition, and glucose metabolism in Parkinson’s disease dementia (PDD)and PD subjects without dementia. Here, we evaluated 11 PDD subjects, 8 PD subjects without dementia, and 24 control subjects.Subjects underwent T1 and T2 MRI, [11C](R)PK11195, [18F]FDG, and [11C]PIB PET scans. Parametric maps of [11C](R)PK11195 bindingpotential, rCMRGlc, and [11C]PIB uptake were interrogated using region of interest and SPM (statistical parametric mapping) analysis. ThePDD patients showed a significant increase of microglial activation in anterior and posterior cingulate, striatum, frontal, temporal, parietal,and occipital cortical regions compared with the controls. The PD subjects also showed a statistically significant increase in microglialactivation in temporal, parietal, and occipital regions. [11C]PIB uptake was marginally increased in PDD and PD. There was a significantreduction in glucose metabolism in PDD and PD. We have also demonstrated pixel-by-pixel correlation between mini-mental stateexamination (MMSE) score and microglial activation and MMSE score and rCMRGlc. In conclusion, we have demonstrated that corticalmicroglial activation and reduced glucose metabolism can be detected early on in this disease spectrum. Significant microglial activationmay be a factor in driving the disease process in PDD. Given this, agents that affect microglial activation could have an influence ondisease progression.
Edison P, Carter SF, Rinne JO, et al., 2013, Comparison of MRI based and PET template based approaches in the quantitative analysis of amyloid imaging with PIB-PET, Neuroimage
RATIONALE:11C]Pittsburgh compound-B (PIB) has been the most widely used positron emission tomography (PET) imaging agent for brain amyloid. Several longitudinal studies evaluating progression of Alzheimer's disease (AD), and numerous therapeutic intervention studies are underway using [11C]PIB PET as an AD biomarker. Quantitative analysis of [11C]PIB data requires the definition of regional volumes of interest. This investigation systematically compared two data analysis routes both using a probabilistic brain atlas with 11 bilateral regions. Route 1 used individually segmented structural magnetic resonance images (MRI) for each subject while Route 2 used a standardised [11C]PIB PET template.METHODS:A total of 54 subjects, 20 with probable Alzheimer's Disease (AD), 14 with amnestic Mild Cognitive Impairment (MCI) and 20 age-matched healthy controls, were scanned at two imaging centres either in London (UK) or in Turku (Finland). For all subjects structural volumetric MRI and [11C]PIB PET scans were acquired. Target-to-cerebellum ratios 40 min to 60 min post injection was used as outcome measures. Regional read outs for grey matter target regions were generated for both routes. Based on a composite neocortical, frontal, posterior cingulate, combined posterior cingulate and frontal cortical regions, scans were categorised into either 'PIB negative' (PIB-) or 'PIB positive' (PIB+) using previously reported cut-off target-to-cerebellar ratios of 1.41, 1.5 and 1.6, respectively.RESULTS:Target-to-cerebellum ratios were greater when defined with a [11C]PIB PET template than with individual MRIs for all cortical regions regardless of diagnosis. This difference was highly significant for controls (p < 0.001, paired samples t-test), less significant for MCIs and borderline for ADs. Assignment of subjects to raised or normal categories was the same with both routes with a 1.6 cut-off while with lower cut off using frontal cortex, and combined frontal cortex and posterior ci
Nordberg A, Carter SF, Rinne J, et al., 2013, A European multicentre PET study of fibrillar amyloid in Alzheimer's disease., Eur J Nucl Med Mol Imaging
PURPOSE:Amyloid PET tracers have been developed for in vivo detection of brain fibrillar amyloid deposition in Alzheimer's disease (AD). To serve as an early biomarker in AD the amyloid PET tracers need to be analysed in multicentre clinical studies.METHODS:In this study 238 [(11)C]Pittsburgh compound-B (PIB) datasets from five different European centres were pooled. Of these 238 datasets, 18 were excluded, leaving [(11)C]PIB datasets from 97 patients with clinically diagnosed AD (mean age 69 ± 8 years), 72 patients with mild cognitive impairment (MCI; mean age 67.5 ± 8 years) and 51 healthy controls (mean age 67.4 ± 6 years) available for analysis. Of the MCI patients, 64 were longitudinally followed for 28 ± 15 months. Most participants (175 out of 220) were also tested for apolipoprotein E (ApoE) genotype.RESULTS:[(11)C]PIB retention in the neocortical and subcortical brain regions was significantly higher in AD patients than in age-matched controls. Intermediate [(11)C]PIB retention was observed in MCI patients, with a bimodal distribution (64 % MCI PIB-positive and 36 % MCI PIB-negative), which was significantly different the pattern in both the AD patients and controls. Higher [(11)C]PIB retention was observed in MCI ApoE ε4 carriers compared to non-ApoE ε4 carriers (p < 0.005). Of the MCI PIB-positive patients, 67 % had converted to AD at follow-up while none of the MCI PIB-negative patients converted.CONCLUSION:This study demonstrated the robustness of [(11)C]PIB PET as a marker of neocortical fibrillar amyloid deposition in brain when assessed in a multicentre setting. MCI PIB-positive patients showed more severe memory impairment than MCI PIB-negative patients and progressed to AD at an estimated rate of 25 % per year. None of the MCI PIB-negative patients converted to AD, and thus PIB negativity had a 100 % negative predictive value for pro
Hyare H, Ramlackhansingh A, Gelosa G, et al., 2012, <SUP>11</SUP>C-PiB PET does not detect PrP-amyloid in prion disease patients including variant Creutzfeldt-Jakob disease, JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, Vol: 83, Pages: 340-341, ISSN: 0022-3050
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- Citations: 5
Edison P, Hinz R, Ramlackhansingh A, et al., 2012, Can target-to-pons ratio be used as a reliable method for the analysis of [(11)C]PIB brain scans?, Neuroimage
RATIONALE: (11)C]PIB is the most widely used PET imaging marker for amyloid in dementia studies. In the majority of studies the cerebellum has been used as a reference region. However, cerebellar amyloid may be present in genetic Alzheimer's (AD), cerebral amyloid angiopathy and prion diseases. Therefore, we investigated whether the pons could be used as an alternative reference region for the analysis of [(11)C]PIB binding in AD. The aims of the study were to: 1) Evaluate the pons as a reference region using arterial plasma input function and Logan graphical analysis of binding. 2) Assess the power of target-to-pons ratios to discriminate controls from AD subjects. 3) Determine the test-retest reliability in AD subjects. 4) Demonstrate the application of target-to-pons ratio in subjects with elevated cerebellar [(11)C]PIB binding. METHODS: 12 sporadic AD subjects aged 65±4.5yrs with a mean MMSE 21.4±4 and 10 age-matched control subjects had [(11)C]PIB PET with arterial blood sampling. Three additional subjects (two subjects with pre-symptomatic presenilin-1 mutation carriers and one probable familial AD) were also studied. Object maps were created by segmenting individual MRIs and spatially transforming the gray matter images into standard stereotaxic MNI space and then superimposing a probabilistic atlas. Cortical [(11)C]PIB binding was assessed with an ROI (region of interest) analysis. Parametric maps of the volume of distribution (V(T)) were generated with Logan analysis. Additionally, parametric maps of the 60-90min target-to-cerebellar ratio (RATIO(CER)) and the 60-90min target-to-pons ratio (RATIO(PONS)) were computed. RESULTS: All three approaches were able to differentiate AD from controls (p<0.0001, nonparametric Wilcoxon rank sum test) in the target regions with RATIO(CER) and RATIO(PONS) differences higher than V(T) with use of an arterial input function. All methods had a good reproducibility (intraclass correlation coefficient>0.83
Corbett A, Pickett J, Burns A, et al., 2012, Drug repositioning for Alzheimer's disease
Existing drugs for Alzheimer's disease provide symptomatic benefit for up to 12 months, but there are no approved disease-modifying therapies. Given the recent failures of various novel disease-modifying therapies in clinical trials, a complementary strategy based on repositioning drugs that are approved for other indications could be attractive. Indeed, a substantial body of preclinical work indicates that several classes of such drugs have potentially beneficial effects on Alzheimer's-like brain pathology, and for some drugs the evidence is also supported by epidemiological data or preliminary clinical trials. Here, we present a formal consensus evaluation of these opportunities, based on a systematic review of published literature. We highlight several compounds for which sufficient evidence is available to encourage further investigation to clarify an optimal dose and consider progression to clinical trials in patients with Alzheimer's disease.
McMurdo MET, Roberts H, Parker S, et al., 2011, Improving recruitment of older people to research through good practice, AGE AND AGEING, Vol: 40, Pages: 659-665, ISSN: 0002-0729
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- Citations: 173
Knight WD, Okello AA, Ryan NS, et al., 2011, Carbon-11-Pittsburgh compound B positron emission tomography imaging of amyloid deposition in presenilin 1 mutation carriers., Brain, Vol: 134, Pages: 293-300
(11)Carbon-Pittsburgh compound B positron emission tomography studies have suggested early and prominent amyloid deposition in the striatum in presenilin 1 mutation carriers. This cross-sectional study examines the (11)Carbon-Pittsburgh compound B positron emission tomography imaging profiles of presymptomatic and mildly affected (mini-mental state examination ≥ 20) carriers of seven presenilin 1 mutations, comparing them with groups of controls and symptomatic sporadic Alzheimer's disease cases. Parametric ratio images representing (11)Carbon-Pittsburgh compound B retention from 60 to 90 min were created using the pons as a reference region and nine regions of interest were studied. We confirmed that increased amyloid load may be detected in presymptomatic presenilin 1 mutation carriers with (11)Carbon-Pittsburgh compound B positron emission tomography and that the pattern of retention is heterogeneous. Comparison of presenilin 1 and sporadic Alzheimer's disease groups revealed significantly greater thalamic retention in the presenilin 1 group and significantly greater frontotemporal retention in the sporadic Alzheimer's disease group. A few individuals with presenilin 1 mutations showed increased cerebellar (11)Carbon-Pittsburgh compound B retention suggesting that this region may not be as suitable a reference region in familial Alzheimer's disease.
Edison P, Hinz R, Brooks DJ, 2011, Technical aspects of amyloid imaging for Alzheimer's disease, ALZHEIMERS RESEARCH & THERAPY, Vol: 3, ISSN: 1758-9193
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- Citations: 8
Edison P, Hinz R, Ramalackansingh A, et al., 2010, Can We Use Pons as a Reference Region for the Analysis of [<SUP>11</SUP>C]PIB PET?, 62nd Annual Meeting of the American-Academy-of-Neurology, Publisher: LIPPINCOTT WILLIAMS & WILKINS, Pages: A337-A337, ISSN: 0028-3878
Rodda J, Okello A, Edison P, et al., 2009, (11)C-PIB PET in subjective cognitive impairment., Eur Psychiatry.
Edison P, Brooks DJ, Turkheimer FE, et al., 2009, Strategies for the generation of parametric images of [<SUP>11</SUP>C]PIB with plasma input functions considering discriminations and reproducibility, NEUROIMAGE, Vol: 48, Pages: 329-338, ISSN: 1053-8119
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- Citations: 20
Okello A, Koivunen J, Edison P, et al., 2009, Conversion of amyloid positive and negative MCI to AD over 3 years An <SUP>11</SUP>C-PIB PET study, NEUROLOGY, Vol: 73, Pages: 754-760, ISSN: 0028-3878
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- Citations: 393
de Llano SRM, Perry R, Waldman A, et al., 2009, In- vivo diagnosis of atypical Alzheimer disease using pathology-sensitive brain imaging, 11C-PIB and short TE spectroscopy MR imaging in Posterior Cortical Atrophy, Publisher: SPRINGER, Pages: 244-244, ISSN: 1619-7070
de Llano SRM, Perry R, Waldman A, et al., 2009, In- vivo diagnosis of atypical Alzheimer disease using pathology-sensitive brain imaging, 11C-PIB and short TE spectroscopy MR imaging in Posterior Cortical Atrophy, EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING, Vol: 36, Pages: S244-S244, ISSN: 1619-7070
Edison P, 2009, Imaging cerebral amyloid in vivo, 5th International Congress on Vascular Dementia, Publisher: ELSEVIER SCIENCE BV, Pages: 263-263, ISSN: 0022-510X
Okello A, Edison P, Archer HA, et al., 2009, Microglial activation and amyloid deposition in mild cognitive impairment A PET study, NEUROLOGY, Vol: 72, Pages: 56-62, ISSN: 0028-3878
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- Citations: 266
Edison P, Rowe CC, Rinne JO, et al., 2008, Amyloid load in Parkinson's disease dementia and Lewy body dementia measured with [11C]PIB positron emission tomography, JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, Vol: 79, Pages: 1331-1338, ISSN: 0022-3050
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- Citations: 319
Tomasi G, Edison P, Bertoldo A, et al., 2008, Novel reference region model reveals increased microglial and reduced vascular binding of 11C-(R)-PK11195 in patients with Alzheimer's disease., J Nucl Med, Vol: 49, Pages: 1249-1256, ISSN: 0161-5505
11C-(R)-PK11195 is a PET radiotracer for the quantification of peripheral benzodiazepine binding sites (PBBSs). The PBBS is a consistent marker of activated microglia, and 11C-(R)-PK11195 has been used to image microglial activity in the diseased brain and in neoplasia. However, the PBBS is also expressed in the brain vasculature (endothelium and smooth muscles), and no evidence, to our knowledge, exists of a change in the vascular PBBS in pathologic brains or of such a change having an effect on the quantification of 11C-(R)-PK11195 binding. To investigate this issue, we have used a modified reference-tissue model (SRTMV) that accounts for tracer vascular activity both in reference and target tissues and applied it for the estimation of binding potential (BP) in a cohort of patients with Alzheimer's disease (AD).
Edison P, Archer HA, Gerhard A, et al., 2008, Microglia, amyloid, and cognition in Alzheimer's disease: An [11C](R)PK11195-PET and [11C]PIB-PET study, Neurobiology of Disease
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