Imperial College London

DrVincenzoLibri

Faculty of MedicineNational Heart & Lung Institute

Honorary Clinical Lecturer
 
 
 
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Contact

 

+44 (0)20 3313 1677v.libri

 
 
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Location

 

NIHR Imperial Clinical Research FacilityICTEM buildingHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

89 results found

Voysey M, Clemens SAC, Madhi SA, Weckx LY, Folegatti PM, Aley PK, Angus B, Baillie VL, Barnabas SL, Bhorat QE, Bibi S, Briner C, Cicconi P, Clutterbuck EA, Collins AM, Cutland CL, Darton TC, Dheda K, Dold C, Duncan CJA, Emary KRW, Ewer KJ, Flaxman A, Fairlie L, Faust SN, Feng S, Ferreira DM, Finn A, Galiza E, Goodman AL, Green CM, Green CA, Greenland M, Hill C, Hill HC, Hirsch I, Izu A, Jenkin D, Joe CCD, Kerridge S, Koen A, Kwatra G, Lazarus R, Libri V, Lillie PJ, Marchevsky NG, Marshall RP, Mendes AVA, Milan EP, Minassian AM, McGregor A, Mujadidi YF, Nana A, Padayachee SD, Phillips DJ, Pittella A, Plested E, Pollock KM, Ramasamy MN, Ritchie AJ, Robinson H, Schwarzbold AV, Smith A, Song R, Snape MD, Sprinz E, Sutherland RK, Thomson EC, Torok ME, Toshner M, Turner DPJ, Vekemans J, Villafana TL, White T, Williams CJ, Douglas AD, Hill AVS, Lambe T, Gilbert SC, Pollard AJet al., 2021, Single-dose administration and the influence of the timing of the booster dose on immunogenicity and efficacy of ChAdOx1 nCoV-19 (AZD1222) vaccine: a pooled analysis of four randomised trials, The Lancet, Vol: 397, Pages: 881-891, ISSN: 0140-6736

BackgroundThe ChAdOx1 nCoV-19 (AZD1222) vaccine has been approved for emergency use by the UK regulatory authority, Medicines and Healthcare products Regulatory Agency, with a regimen of two standard doses given with an interval of 4–12 weeks. The planned roll-out in the UK will involve vaccinating people in high-risk categories with their first dose immediately, and delivering the second dose 12 weeks later. Here, we provide both a further prespecified pooled analysis of trials of ChAdOx1 nCoV-19 and exploratory analyses of the impact on immunogenicity and efficacy of extending the interval between priming and booster doses. In addition, we show the immunogenicity and protection afforded by the first dose, before a booster dose has been offered.MethodsWe present data from three single-blind randomised controlled trials—one phase 1/2 study in the UK (COV001), one phase 2/3 study in the UK (COV002), and a phase 3 study in Brazil (COV003)—and one double-blind phase 1/2 study in South Africa (COV005). As previously described, individuals 18 years and older were randomly assigned 1:1 to receive two standard doses of ChAdOx1 nCoV-19 (5 × 1010 viral particles) or a control vaccine or saline placebo. In the UK trial, a subset of participants received a lower dose (2·2 × 1010 viral particles) of the ChAdOx1 nCoV-19 for the first dose. The primary outcome was virologically confirmed symptomatic COVID-19 disease, defined as a nucleic acid amplification test (NAAT)-positive swab combined with at least one qualifying symptom (fever ≥37·8°C, cough, shortness of breath, or anosmia or ageusia) more than 14 days after the second dose. Secondary efficacy analyses included cases occuring at least 22 days after the first dose. Antibody responses measured by immunoassay and by pseudovirus neutralisation were exploratory outcomes. All cases of COVID-19 with a NAAT-positive swab were adjudicated for inclusion in the analysis by a masked

Journal article

Voysey M, Clemens SAC, Madhi SA, Weckx LY, Folegatti PM, Aley PK, Angus B, Baillie VL, Barnabas SL, Bhorat QE, Bibi S, Briner C, Cicconi P, Collins AM, Colin-Jones R, Cutland CL, Darton TC, Dheda K, Duncan CJA, Emary KRW, Ewer KJ, Fairlie L, Faust SN, Feng S, Ferreira DM, Finn A, Goodman AL, Green CM, Green CA, Heath PT, Hill C, Hill H, Hirsch I, Hodgson SHC, Izu A, Jackson S, Jenkin D, Joe CCD, Kerridge S, Koen A, Kwatra G, Lazarus R, Lawrie AM, Lelliott A, Libri V, Lillie PJ, Mallory R, Mendes AVA, Milan EP, Minassian AM, McGregor A, Morrison H, Mujadidi YF, Nana A, O'Reilly PJ, Padayachee SD, Pittella A, Plested E, Pollock KM, Ramasamy MN, Rhead S, Schwarzbold AV, Singh N, Smith A, Song R, Snape MD, Sprinz E, Sutherland RK, Tarrant R, Thomson EC, Török ME, Toshner M, Turner DPJ, Vekemans J, Villafana TL, Watson MEE, Williams CJ, Douglas AD, Hill AVS, Lambe T, Gilbert SC, Pollard AJ, Oxford COVID Vaccine Trial Groupet al., 2021, Safety and efficacy of the ChAdOx1 nCoV-19 vaccine (AZD1222) against SARS-CoV-2: an interim analysis of four randomised controlled trials in Brazil, South Africa, and the UK, The Lancet, Vol: 397, Pages: 99-111, ISSN: 0140-6736

BACKGROUND: A safe and efficacious vaccine against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), if deployed with high coverage, could contribute to the control of the COVID-19 pandemic. We evaluated the safety and efficacy of the ChAdOx1 nCoV-19 vaccine in a pooled interim analysis of four trials. METHODS: This analysis includes data from four ongoing blinded, randomised, controlled trials done across the UK, Brazil, and South Africa. Participants aged 18 years and older were randomly assigned (1:1) to ChAdOx1 nCoV-19 vaccine or control (meningococcal group A, C, W, and Y conjugate vaccine or saline). Participants in the ChAdOx1 nCoV-19 group received two doses containing 5 × 1010 viral particles (standard dose; SD/SD cohort); a subset in the UK trial received a half dose as their first dose (low dose) and a standard dose as their second dose (LD/SD cohort). The primary efficacy analysis included symptomatic COVID-19 in seronegative participants with a nucleic acid amplification test-positive swab more than 14 days after a second dose of vaccine. Participants were analysed according to treatment received, with data cutoff on Nov 4, 2020. Vaccine efficacy was calculated as 1 - relative risk derived from a robust Poisson regression model adjusted for age. Studies are registered at ISRCTN89951424 and ClinicalTrials.gov, NCT04324606, NCT04400838, and NCT04444674. FINDINGS: Between April 23 and Nov 4, 2020, 23 848 participants were enrolled and 11 636 participants (7548 in the UK, 4088 in Brazil) were included in the interim primary efficacy analysis. In participants who received two standard doses, vaccine efficacy was 62·1% (95% CI 41·0-75·7; 27 [0·6%] of 4440 in the ChAdOx1 nCoV-19 group vs71 [1·6%] of 4455 in the control group) and in participants who received a low dose followed by a standard dose, efficacy was 90·0% (67·4-97·0; three [0·2%] of 1367 vs 30 [2·2%] of 1374; pin

Journal article

Mullin S, Smith L, Lee K, D'Souza G, Woodgate P, Elflein J, Hällqvist J, Toffoli M, Streeter A, Hosking J, Heywood WE, Khengar R, Campbell P, Hehir J, Cable S, Mills K, Zetterberg H, Limousin P, Libri V, Foltynie T, Schapira AHVet al., 2020, Ambroxol for the Treatment of Patients With Parkinson Disease With and Without Glucocerebrosidase Gene Mutations: A Nonrandomized, Noncontrolled Trial., JAMA Neurol, Vol: 77, Pages: 427-434

Importance: Mutations of the glucocerebrosidase gene, GBA1 (OMIM 606463), are the most important risk factor for Parkinson disease (PD). In vitro and in vivo studies have reported that ambroxol increases β-glucocerebrosidase (GCase) enzyme activity and reduces α-synuclein levels. These observations support a potential role for ambroxol therapy in modifying a relevant pathogenetic pathway in PD. Objective: To assess safety, tolerability, cerebrospinal fluid (CSF) penetration, and target engagement of ambroxol therapy with GCase in patients with PD with and without GBA1 mutations. Interventions: An escalating dose of oral ambroxol to 1.26 g per day. Design, Setting, and Participants: This single-center open-label noncontrolled clinical trial was conducted between January 11, 2017, and April 25, 2018, at the Leonard Wolfson Experimental Neuroscience Centre, a dedicated clinical research facility and part of the University College London Queen Square Institute of Neurology in London, United Kingdom. Participants were recruited from established databases at the Royal Free London Hospital and National Hospital for Neurology and Neurosurgery in London. Twenty-four patients with moderate PD were evaluated for eligibility, and 23 entered the study. Of those, 18 patients completed the study; 1 patient was excluded (failed lumbar puncture), and 4 patients withdrew (predominantly lumbar puncture-related complications). All data analyses were performed from November 1 to December 14, 2018. Main Outcomes and Measures: Primary outcomes at 186 days were the detection of ambroxol in the CSF and a change in CSF GCase activity. Results: Of the 18 participants (15 men [83.3%]; mean [SD] age, 60.2 [9.7] years) who completed the study, 17 (8 with GBA1 mutations and 9 without GBA1 mutations) were included in the primary analysis. Between days 0 and 186, a 156-ng/mL increase in the level of ambroxol in CSF (lower 95% confidence limit, 129 ng/mL; P < .001) was ob

Journal article

Reetz K, Hilgers R-D, Isfort S, Dohmen M, Didszun C, Fedosov K, Kistermann J, Mariotti C, Durr A, Boesch S, Klopstock T, Rodríguez de Rivera Garrido FJ, Schöls L, Klockgether T, Pandolfo M, Korinthenberg R, Lavin P, Molenberghs G, Libri V, Giunti P, Festenstein R, Schulz JB, EFACTS or NICOFA study groupet al., 2019, Protocol of a randomized, double-blind, placebo-controlled, parallel-group, multicentre study of the efficacy and safety of nicotinamide in patients with Friedreich ataxia (NICOFA), Neurological Research and Practice, Vol: 1, ISSN: 2524-3489

Introduction: Currently, no treatment that delays with the progression of Friedreich ataxia is available. In the majority of patients Friedreich ataxia is caused by homozygous pathological expansion of GAA repeats in the first intron of the FXN gene. Nicotinamide acts as a histone deacetylase inhibitor. Dose escalation studies have shown, that short term treatment with dosages of up to 4 g/day increase the expression of FXN mRNA and frataxin protein up to the levels of asymptomatic heterozygous gene carriers. The long-term effects and the effects on clinical endpoints, activities of daily living and quality of life are unknown. Methods: The aim of the NICOFA study is to investigate the efficacy and safety of nicotinamide for the treatment of Friedreich ataxia over 24 months. An open-label dose adjustment wash-in period with nicotinamide (phase A: weeks 1-4) to the individually highest tolerated dose of 2-4 g nicotinamide/day will be followed by a 2 (nicotinamide group): 1 (placebo group) randomization (phase B: weeks 5-104). In the nicotinamide group, patients will continue with their individually highest tolerated dose between 2 and 4 g/d per os once daily and the placebo group patients will be receiving matching placebo. Safety assessments will consist of monitoring and recording of all adverse events and serious adverse events, regular monitoring of haematology, blood chemistry and urine values, regular measurement of vital signs and the performance of physical examinations including cardiological signs. The primary outcome is the change in the Scale for the Assessment and Rating of Ataxia (SARA) over time as compared with placebo in patients with Friedreich ataxia based on the linear mixed effect model (LMEM) model. Secondary endpoints are measures of quality of life, functional motor and cognitive measures, clinician's and patient's global impression-change scales as well as the up-regulation of the frataxin protein level, safety and

Journal article

Mauricio R, Benn C, Davis J, Dawson G, Dawson LA, Evans A, Fox N, Gallacher J, Hutton M, Isaac J, Jones DNC, Jones L, Lalli G, Libri V, Lovestone S, Moody C, Noble W, Perry H, Pickett J, Reynolds D, Ritchie C, Rohrer JD, Routledge C, Rowe J, Snyder H, Spires-Jones T, Swartz J, Truyen L, Whiting P, Therapeutics for Dementia Consortiumet al., 2019, Tackling gaps in developing life-changing treatments for dementia., Alzheimers Dement (N Y), Vol: 5, Pages: 241-253

Since the G8 dementia summit in 2013, a number of initiatives have been established with the aim of facilitating the discovery of a disease-modifying treatment for dementia by 2025. This report is a summary of the findings and recommendations of a meeting titled "Tackling gaps in developing life-changing treatments for dementia", hosted by Alzheimer's Research UK in May 2018. The aim of the meeting was to identify, review, and highlight the areas in dementia research that are not currently being addressed by existing initiatives. It reflects the views of leading experts in the field of neurodegeneration research challenged with developing a strategic action plan to address these gaps and make recommendations on how to achieve the G8 dementia summit goals. The plan calls for significant advances in (1) translating newly identified genetic risk factors into a better understanding of the impacted biological processes; (2) enhanced understanding of selective neuronal resilience to inform novel drug targets; (3) facilitating robust and reproducible drug-target validation; (4) appropriate and evidence-based selection of appropriate subjects for proof-of-concept clinical trials; (5) improving approaches to assess drug-target engagement in humans; and (6) innovative approaches in conducting clinical trials if we are able to detect disease 10-15 years earlier than we currently do today.

Journal article

Owen DRJ, Fan J, Campioli E, Venugopal S, Midzak A, Daly E, Harlay A, Issop L, Libri V, Kalogiannopoulou D, Oliver E, Gallego-Colon E, Colasanti A, Huson L, Rabiner EA, Suppiah P, Essagian C, Matthews PM, Papadopoulos Vet al., 2017, TSPO mutations in rats and a human polymorphism impair the rate of steroid synthesis, Biochemical Journal, Vol: 474, Pages: 3985-3999, ISSN: 1470-8728

The 18 kDa translocator protein (TSPO) is a ubiquitous conserved outer mitochondrial membrane protein implicated in numerous cell and tissue functions, including steroid hormone biosynthesis, respiration, cell proliferation, and apoptosis. TSPO binds with high affinity to cholesterol and numerous compounds, is expressed at high levels in steroid-synthesizing tissues, and mediates cholesterol import into mitochondria, which is the rate-limiting step in steroid formation. In humans, the rs6971 polymorphism on the TSPO gene leads to an amino acid substitution in the fifth transmembrane loop of the protein, which is where the cholesterol-binding domain of TSPO is located, and this polymorphism has been associated with anxiety-related disorders. However, recent knockout mouse models have provided inconsistent conclusions of whether TSPO is directly involved in steroid synthesis. In this report, we show that TSPO deletion mutations in rat and its corresponding rs6971 polymorphism in humans alter adrenocorticotropic hormone-induced plasma corticosteroid concentrations. Rat tissues examined show increased cholesteryl ester accumulation, and neurosteroid formation was undetectable in homozygous rats. These results also support a role for TSPO ligands in diseases with steroid-dependent stress and anxiety elements.

Journal article

quinn K, Traboni C, Dily Penchala S, bouliotis G, doyle N, libri V, Khoo S, ashby D, weber J, Nicosia A, Cortese R, Pessi A, Winston Aet al., 2017, A first-in-human study of the novel HIV-fusion inhibitor C34-PEG4-Chol., Scientific Reports, Vol: 7, ISSN: 2045-2322

Abstract:Long-acting injectable antiretroviral (LA-ARV) drugs with low toxicity profiles and propensity for drug-drug interactions are a goal for future ARV regimens. C34-PEG4-Chol is a novel cholesterol tagged LA HIV-fusion-inhibitor (FI). We assessed pre-clinical toxicology and first-in-human administration of C34-PEG4-Chol. Pre-clinical toxicology was conducted in 2 species. HIV-positive men were randomised to a single subcutaneous dose of C34-PEG4-Chol at incrementing doses or placebo. Detailed clinical (including injection site reaction (ISR) grading), plasma pharmacokinetic (time-to-minimum-effective-concentration (MEC, 25ng/mL) and pharmacodynamic (plasma HIV RNA) parameters were assessed. In both mice and dogs, no-observed-adverse effect level (NOAEL) was observed at a 12 mg/kg/dose after two weeks. Of 5 men enrolled, 3 received active drug (10mg, 10mg and 20mg). In 2 individuals grade 3 ISR occurred and the study was halted. Both ISR emerged within 12 hours of active drug dosing. No systemic toxicities were observed. The time-to-MEC was > 72 and >96 hours after 10 and 20 mg dose, respectively, and mean change in HIV RNA was -0.9 log10 copies/mL. These human pharmacodynamic and pharmacokinetic data, although limited to 3 subjects, of C34-PEG-4-Chol suggest continuing evaluation of this agent as a LA-ARV. However, alternative administration routes must be explored.

Journal article

Quinn K, Bouliotis G, Doyle N, Winston A, Ashby D, Weber J, Libri V, Amara A, Back D, Penchala SD, Khoo S, Nelson M, Jones R, Cortese R, Pessi Aet al., 2016, A first-in-human study, in HIV-positive men, of the novel HIV-fusion inhibitor C34-PEG4-Chol, 22nd Annual Conference of the British HIV Association (BHIVA), Publisher: Wiley, Pages: 18-18, ISSN: 1464-2662

Conference paper

Libri V, Yandim C, Athanasopoulos S, Loyse N, Natisvili T, Law PP, Chan PK, Mohammad T, Mauri M, Tam KT, Leiper J, Piper S, Ramesh A, Parkinson MH, Huson L, Giunti P, Festenstein Ret al., 2014, Epigenetic and neurological effects and safety of high-dose nicotinamide in patients with Friedreich's ataxia: an exploratory, open-label, dose-escalation study, The Lancet, Vol: 384, Pages: 504-513, ISSN: 0140-6736

BackgroundFriedreich's ataxia is a progressive degenerative disorder caused by deficiency of the frataxin protein. Expanded GAA repeats within intron 1 of the frataxin (FXN) gene lead to its heterochromatinisation and transcriptional silencing. Preclinical studies have shown that the histone deacetylase inhibitor nicotinamide (vitamin B3) can remodel the pathological heterochromatin and upregulate expression of FXN. We aimed to assess the epigenetic and neurological effects and safety of high-dose nicotinamide in patients with Friedreich's ataxia.MethodsIn this exploratory, open-label, dose-escalation study in the UK, male and female patients (aged 18 years or older) with Friedreich's ataxia were given single doses (phase 1) and repeated daily doses of 2–8 g oral nicotinamide for 5 days (phase 2) and 8 weeks (phase 3). Doses were gradually escalated during phases 1 and 2, with individual maximum tolerated doses used in phase 3. The primary outcome was the upregulation of frataxin expression. We also assessed the safety and tolerability of nicotinamide, used chromatin immunoprecipitation to investigate changes in chromatin structure at the FXN gene locus, and assessed the effect of nicotinamide treatment on clinical scales for ataxia. This study is registered with ClinicalTrials.gov, number NCT01589809.FindingsNicotinamide was generally well tolerated; the main adverse event was nausea, which in most cases was mild, dose-related, and resolved spontaneously or after dose reduction, use of antinausea drugs, or both. Phase 1 showed a dose-response relation for proportional change in frataxin protein concentration from baseline to 8 h post-dose, which increased with increasing dose (p=0·0004). Bayesian analysis predicted that 3·8 g would result in a 1·5-times increase and 7·5 g in a doubling of frataxin protein concentration. Phases 2 and 3 showed that daily dosing at 3·5–6 g resulted in a sustained and significant (p<0&m

Journal article

Libri V, Gibbs JSR, Pinato DJ, Iddamalgoda T, Khengar RH, Gin-Sing W, Huson L, Anand Pet al., 2014, Capsaicin 8% patch for treprostinil subcutaneous infusion site pain in pulmonary hypertension patients, BRITISH JOURNAL OF ANAESTHESIA, Vol: 112, Pages: 337-347, ISSN: 0007-0912

Journal article

Owen DR, Guo Q, Kalk NJ, Colasanti A, Kalogiannopoulou D, Dimber R, Lewis YL, Libri V, Barletta J, Ramada-Magalhaes J, Kamalakaran A, Nutt DJ, Passchier J, Matthews PM, Gunn RN, Rabiner EAet al., 2014, Eratum: Determination of [ 11 C]PBR28 binding potential in vivo: A first human TSPO blocking study (Journal of Cerebral Blood Flow and Metabolism (2014) 34 (1256)), Journal of Cerebral Blood Flow and Metabolism, Vol: 34, ISSN: 0271-678X

Journal article

Owen D, Guo Q, Colasanti A, Kalk N, Kalogiannopoulou D, Libri V V, Lewis Y, Matthews PM, Gunn R, Rabiner Eet al., 2013, Determination of [11C]PBR28 binding potential in vivo: A first human TSPO occupancy study.

Journal article

Libri V, 2013, Effects of Capsaicin 8% Patches on SC Treprostinil Infusion Site Pain: Experience from a Randomised Double-Blinded Phase IIa Clinical Trial., 8th John Vane Memorial conference on Prostacyclin Science and Pulmonary Vascular Disease

Conference paper

Libri V, Brown AP, Gambarota G, Haddad G, Shields GS, Dawes H, Pinato DJ, Hoffman E, Elliot PJ, Vlasuk GP, Jacobson E, Wilkins MR, Matthews PMet al., 2012, A Pilot Randomized, Placebo Controlled, Double Blind Phase I Trial of the Novel SIRT1 Activator SRT2104 in Elderly Volunteers, PLoS ONE, Vol: 7, ISSN: 1932-6203

Background:SRT2104 has been developed as a selective small molecule activator of SIRT1, a NAD+-dependent deacetylaseinvolved in the regulation of energy homeostasis and the modulation of various metabolic pathways, including glucosemetabolism, oxidative stress and lipid metabolism. SIRT1 has been suggested as putative therapeutic target in multiple age-related diseases including type 2 diabetes and dyslipidemias. We report the first clinical trial of SRT2104 in elderlyvolunteers.Methods:Oral doses of 0.5 or 2.0 g SRT2104 or matching placebo were administered once daily for 28 days.Pharmacokinetic samples were collected through 24 hours post-dose on days 1 and 28. Multiple pharmacodynamicendpoints were explored with oral glucose tolerance tests (OGTT), serum lipid profiles, magnetic resonance imaging (MRI)for assessment of whole body visceral and subcutaneous fat, maximal aerobic capacity test and muscle 31P magneticresonance spectroscopy (MRS) for estimation of mitochondrial oxidative capacity.Results:SRT2104 was generally safe and well tolerated. Pharmacokinetic exposure increased less than dose-proportionally.Mean Tmax was 2–4 hours with elimination half-life of 15–20 hours. Serum cholesterol, LDL levels and triglyceridesdecreased with treatment. No significant changes in OGTT responses were observed. 31P MRS showed trends for morerapid calculated adenosine diphosphate (ADP) and phosphocreatine (PCr) recoveries after exercise, consistent withincreased mitochondrial oxidative phosphorylation.Conclusions:SRT2104 can be safely administered in elderly individuals and has biological effects in humans that areconsistent with SIRT1 activation. The results of this study support further development of SRT2104 and may be useful indose selection for future clinical trials in patients.

Journal article

Pinato DJ, Stavraka C, Tanner M, Esson A, Jacobson EW, Wilkins MR, Libri Vet al., 2012, Clinical, Ethical and Financial Implications of Incidental Imaging Findings: Experience from a Phase I Trial inHealthy Elderly Volunteers, Plos One, Vol: 7

Stavraka1, Mark Tanner2, Audrey Esson1, Eric W. Jacobson3, Martin R. Wilkins1,Vincenzo Libri1*

Journal article

Lythe KE, Williams SCR, Anderson C, Libri V, Mehta MAet al., 2012, Frontal and parietal activity after sleep deprivation is dependent on task difficulty and can be predicted by the fMRI response after normal sleep, BEHAVIOURAL BRAIN RESEARCH, Vol: 233, Pages: 62-70, ISSN: 0166-4328

Journal article

Libri V, 2010, Developing Products for Rare Diseases: Assessing financial and clinical challenges to navigate the way forward, Evolution Summit 2010

Conference paper

Libri V, 2010, Experimental medicine endpoints in early-phase clinical trials for CNS indications, Forty Years of Advances in Pharmacology, Editors: Nistico, Rotiroti, De Sarro, Pages: 152-165

Book chapter

Devanand DP, Mikhno A, Pelton GH, Cuasay K, Pradhaban G, Dileep Kumar JS, Upton N, Lai R, Gunn RN, Libri V, Liu X, van Heertum R, Mann JJ, Parsey RVet al., 2010, Pittsburgh compound B (11C-PIB) and fluorodeoxyglucose (18 F-FDG) PET in patients with Alzheimer disease, mild cognitive impairment, and healthy controls, J Geriatr Psychiatry Neurol, Vol: 23, Pages: 185-198, ISSN: 0891-9887

Amyloid load in the brain using Pittsburgh compound B ((11)C-PIB) positron emission tomography (PET) and cerebral glucose metabolism using fluorodeoxyglucose ((18)F-FDG) PET were evaluated in patients with mild Alzheimer disease (AD, n = 18), mild cognitive impairment (MCI, n = 24), and controls (CTR, n = 18). ( 11)C-PIB binding potential (BP(ND)) was higher in prefrontal cortex, cingulate, parietal cortex, and precuneus in AD compared to CTR or MCI and in prefrontal cortex for MCI compared to CTR. For (18)F-FDG, regional cerebral metabolic rate for glucose (rCMRGlu) was decreased in precuneus and parietal cortex in AD compared to CTR and MCI, with no MCI-CTR differences. For the AD-CTR comparison, precuneus BP(ND) area under the receiver operating characteristic (ROC) curve (AUC) was 0.938 and parietal cortex rCMRGlu AUC was 0.915; for the combination, AUC was 0.989. ( 11)C-PIB PET BP(ND) clearly distinguished diagnostic groups and combined with (18)F-FDG PET rCMRGlu, this effect was stronger. These PET techniques provide complementary information in strongly distinguishing diagnostic groups in cross-sectional comparisons that need testing in longitudinal studies.

Journal article

Thompson PW, Ye L, Morgenstern JL, Sue L, Beach TG, Judd DJ, Shipley NJ, Libri V, Lockhart Aet al., 2009, Interaction of the amyloid imaging tracer FDDNP with hallmark Alzheimer’s disease pathologies, Journal of Neurochemistry, Vol: 109, Pages: 623-630

Journal article

Devanand DP, Mikhno A, Pelton GH, Cuasay K, Kumar JSD, Upton N, Lai R, Gunn R, Libri V, Mann JJ, Parsey RVet al., 2009, Comparison of Pittsburgh compound B (11C-PIB) and fluorodeoxyglucose (18F-FDG) PET in patients with Alzheimer's disease, mild cognitive impairment, and healthy controls

Conference paper

Ye L, Velasco A, Fraser G, Beach G, Sue L, Osredkar T, Libri V, Spillantini MG, Goedert M, Lockhart Aet al., 2008, In vitro high affinity alpha-synuclein binding sites for the amyloid imaging agent PIB are not matched by binding to Lewy bodies in post-mortem human brain, Journal of Neurochemistry, Vol: 105, Pages: 1428-1437

Journal article

Mikhno A, Devanand DP, Parsey R, Pelton GH, Cuasay K, Kumar JSD, Upton N, Lai R, Pradhaban G, Libri V, Gunn RN, Mann JJet al., 2008, The use of voxel-based analysis of [11C]PIB scans for the diagnosis of Alzheimer’s disease, Journal of Nuclear Medicine, Vol: 49, Pages: 1262-1269

Journal article

Jones N, Messenger MJ, ONeill MJ, Oldershaw A, Gilmour G, Simmons RMA, Iyengar S, Libri V, Tricklebank M, Williams SCRet al., 2008, AMPA receptor potentiation can prevent ethanol-induced intoxication, Neuropsychopharmacology, Vol: 33

Journal article

Pan M, Chuah LYM, Chen A, Chong D, Rekshan W, Tan JC, Lay RYK, Libri V, Chee MWLet al., 2008, The neurocognitive effects of donepezil on visual short-term memory capacity following 24 Hours of sleep deprivation, Pages: T507-T508

Conference paper

Pan M, Chuah LYM, Chong D, Tan JC, Rekshan W, Chen A, Lai RYK, Libri V, Chee MWLet al., 2008, The neurocognitive benefits of donepezil on episodic memory in young, healthy individuals following 24 Hours of sleep deprivation, Pages: T506-T507

Conference paper

Lai RY, Gregory S, Hall D, Kenny G, Caceres A, Libri V, Williams SCR, Zelaya FO, Mehta MAet al., 2008, A novel potent histamine H3 receptor antagonist produces discrete changes in brain activity during learning and episodic memory: Implications for cognitive enhancement, Pages: T503-T504

Conference paper

Devanand DP, Mikhno A, Pelton GH, Cuasay K, Kumar JSD, Tabert MH, Pradhaban G, Upton N, Lai R, Libri V, Gunn RN, Mann JJ, Parsey RVet al., 2008, PET amyloid imaging with Pittsburgh Compound B in Alzheimer's disease

Conference paper

Mikhno A, Devanand DP, Pelton GH, Cuasay K, Gunn RN, Upton N, Libri V, Mann JJ, Parsey RVet al., 2008, Voxel-based analysis of C11 Pittsburgh compound B for diagnosing Alzheimer's disease

Conference paper

Lockhart A, Lamb JR, Osredkar T, Sue LI, Joyce JN, Ye L, Libri V, Leppert D, Beach TGet al., 2007, PIB is a non-specific imaging marker of amyloid-beta (A beta) peptide-related cerebral amyloidosis, BRAIN, Vol: 130, Pages: 2607-2615, ISSN: 0006-8950

Journal article

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