270 results found
Lee J-Y, Martin-Bastida A, Murueta-Goyena A, et al., 2022, Multimodal brain and retinal imaging of dopaminergic degeneration in Parkinson disease, NATURE REVIEWS NEUROLOGY, Vol: 18, Pages: 203-220, ISSN: 1759-4758
Xing Y, Sapuan AH, Martin-Bastida A, et al., 2022, Neuromelanin-MRI to Quantify and Track Nigral Depigmentation in Parkinson's Disease: A Multicenter Longitudinal Study Using Template-Based Standardized Analysis, MOVEMENT DISORDERS, ISSN: 0885-3185
Hannaway N, Lao-Kaim NP, Martin-Bastida A, et al., 2021, Longitudinal changes in movement-related functional MRI activity in Parkinson's disease patients, PARKINSONISM & RELATED DISORDERS, Vol: 87, Pages: 61-69, ISSN: 1353-8020
Tarkin JM, Corovic A, Wall C, et al., 2020, Positron emission tomography imaging in cardiovascular disease, HEART, Vol: 106, Pages: 1712-1718, ISSN: 1355-6037
Zeng Z, Roussakis A-A, Lao-Kaim NP, et al., 2020, Astrocytes in Parkinson's disease: from preclinical assays to in vivo imaging and therapeutic probes, NEUROBIOLOGY OF AGING, Vol: 95, Pages: 264-270, ISSN: 0197-4580
Porter E, Roussakis A-A, Lao-Kaim NP, et al., 2020, Multimodal dopamine transporter (DAT) imaging and magnetic resonance imaging (MRI) to characterise early Parkinson's disease, PARKINSONISM & RELATED DISORDERS, Vol: 79, Pages: 26-33, ISSN: 1353-8020
Roussakis A-A, Zeng Z, Lao-Kaim NP, et al., 2020, Parkinson's disease laterality: a(11)C-PE2I PET imaging study, JOURNAL OF NEUROLOGY, Vol: 268, Pages: 582-589, ISSN: 0340-5354
Davies R, Babu-Narayan S, 2020, Deep learning in congenital heart disease imaging: hope but not haste, HEART, Vol: 106, Pages: 960-961, ISSN: 1355-6037
Peters S, Gallo V, Vineis P, et al., 2020, Alcohol consumption and risk of Parkinson's disease: data from a large prospective European cohort, Movement Disorders, Vol: 35, Pages: 1258-1263, ISSN: 0885-3185
BackgroundParkinson's disease (PD) etiology is not well understood. Reported inverse associations with smoking and coffee consumption prompted the investigation of alcohol consumption as a risk factor, for which evidence is inconclusive.ObjectiveTo assess the associations between alcohol consumption and PD risk.MethodsWithin NeuroEPIC4PD, a prospective European population‐based cohort, 694 incident PD cases were ascertained from 209,998 PD‐free participants. Average alcohol consumption at different time points was self‐reported at recruitment. Cox regression hazard ratios were estimated for alcohol consumption and PD occurrence.ResultsNo associations between baseline or lifetime total alcohol consumption and PD risk were observed. Men with moderate lifetime consumption (5–29.9 g/day) were at ~50% higher risk compared with light consumption (0.1–4.9 g/day), but no linear exposure–response trend was observed. Analyses by beverage type also revealed no associations with PD.ConclusionOur data reinforce previous findings from prospective studies showing no association between alcohol consumption and PD risk. © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
Altmann DM, Douek DC, Boyton RJ, 2020, What policy makers need to know about COVID-19 protective immunity, The Lancet, Vol: 395, Pages: 1527-1529, ISSN: 0140-6736
Jenkins P, Roussakis A-A, De Simoni S, et al., 2020, Distinct dopaminergic abnormalities in traumatic brain injury and Parkinson’s disease, Journal of Neurology, Neurosurgery and Psychiatry, Vol: 91, Pages: 631-637, ISSN: 0022-3050
Objective: Traumatic brain injury (TBI) and REM behavioural disorder (RBD) are risk factors for Parkinson’s disease (PD). Dopaminergic abnormalities are often seen after TBI, but patients usually lack parkinsonian features. We test whether TBI, PD and RBD have distinct striatal dopamine abnormalities using dopamine transporter imaging. Methods: 123I-ioflupane SPECT scans were used in a cross-sectional study to measure dopamine transporter (DaT) levels in moderate/severe TBI, healthy controls, early PD and RBD patients. Caudate and putamen DaT, putamen-to-caudate ratios and left-right symmetry of DaT were compared.Results: 108 participants (43 TBI, 26 PD, 8 RBD, 31 controls) were assessed. Early PD patients scored significantly higher on the UPDRS motor subscale than other groups. TBI and PD patients had reduced DaT levels in the caudate (12.2% and 18.7% respectively) and putamen (9.0% and 42.6% respectively) compared to controls. RBD patients had reduced DaT levels in the putamen (12.8%) but not in the caudate compared to controls. PD and TBI patients showed distinct patterns of DaT reduction, with PD patients showing a lower putamen-to-caudate ratio. DaT asymmetry was greater in the PD group than other groups. Conclusions: The results show that early PD and TBI patients have distinct patterns of striatal dopamine abnormalities. Early PD and moderate/severe TBI patients showed similar reductions in caudate DaT binding, but PD patients showed a greater reduction in putamen DaT and a lower putamen-to-caudate ratio. The results suggest that parkinsonian motor signs are absent in these TBI patients because of relatively intact putaminal dopamine levels.
Roussakis A-A, Patel NH, Gennaro M, et al., 2020, The role of semi-quantification of 123I-FP-CIT SPECT scans in improving the quality of reporting, 6th Congress of the European-Academy-of-Neurology (EAN), Publisher: WILEY, Pages: 973-973, ISSN: 1351-5101
Adilbekova B, Lin Y, Yengel E, et al., 2020, Liquid phase exfoliation of MoS2 and WS2 in aqueous ammonia and their application in highly efficient organic solar cells, JOURNAL OF MATERIALS CHEMISTRY C, Vol: 8, Pages: 5259-5264, ISSN: 2050-7526
Li W, Lao-Kaim NP, Roussakis A-A, et al., 2020, Longitudinal functional connectivity changes related to dopaminergic decline in Parkinson's disease, NEUROIMAGE-CLINICAL, Vol: 28, ISSN: 2213-1582
van Eimeren T, Antonini A, Berg D, et al., 2019, Neuroimaging biomarkers for clinical trials in atypical parkinsonian disorders: Proposal for a Neuroimaging Biomarker Utility System, ALZHEIMER'S & DEMENTIA: DIAGNOSIS, ASSESSMENT & DISEASE MONITORING, Vol: 11, Pages: 301-309
Roussakis A, Towey D, Gennaro M, et al., 2019, Parkinson’s disease dyskinesias possibly relate to greater dopamine transporter losses in the putamen over time, Journal of Neurology & Experimental Neuroscience, Vol: 5, Pages: S6-S11, ISSN: 2469-407X
The pathophysiology of levodopa-induced dyskinesias in Parkinson’s disease is incompletely understood. This study was designed to investigate in Parkinson’s patients, whether time-related changes in striatal dopamine transporter availability are associated to the appearance of dyskinesias. 15 Parkinson’s patients had dopamine transporter-specific SPECT imaging with 123I-FP-CIT twice: at baseline (when they were drug naïve) and at follow-up (6.31±2.29 years from baseline), and were followed up clinically every six months. At the end of the study, patients were divided in two groups according to whether they had developed dyskinesias or not. Semi-quantification of 123I-FP-CIT data was performed using the occipital cortex as the reference region. Specific binding ratios were calculated for the putamen and the caudate. During the clinical follow-up, all Parkinson’s patients were treated pharmaceutically. 8 patients developed dyskinesias, while 7 remained nondyskinetic. At baseline, the two groups had similar 123I-FP-CIT specific binding ratio values for the putamen and the caudate (p>0.05). Also, between-group differences in age, disease duration, and Hoehn & Yahr scores were not statistically significant. Over-time, the putaminal 123I-FP-CIT specific binding ratio values in the dyskinetic group decreased significantly (p<0.01). The nondyskinetic patients had smaller reductions (p<0.05) during the same period of time. At follow-up, the dyskinetic patients had significantly higher Hoehn & Yahr scores (p<0.01) and were taking higher levodopa equivalent doses (p<0.001), as compared to the nondyskinetic patients. The development of Parkinson’s dyskinesias is related to a faster progression rate, as reflected by marked putaminal dopamine transporter decreases.
Piccini P, Pagano G, Politis M, 2019, Comparison of phosphodiesterase 10A and dopamine transporter levels as markers of disease burden in early Parkinson's disease, Movement Disorders, Vol: 34, Pages: 1505-1515, ISSN: 0885-3185
BackgroundRecent work has shown loss of phosphodiesterase 10A levels in middle‐stage and advanced treated patients with PD, which was associated with motor symptom severity.ObjectivesTo assess phosphodiesterase 10A levels in early PD and compare with loss of dopamine transporter as markers of disease burden.MethodsSeventy‐eight subjects were included in this study (17 early de novo, 15 early l‐dopa–treated, 24 moderate‐advanced l‐dopa–treated patients with PD, and 22 healthy controls). All participants underwent [11C]IMA107 PET, [11C]PE2I PET, and 3‐Tesla MRI scan.ResultsEarly de novo PD patients showed loss of [11C]IMA107 and of [11C]PE2I binding in caudate and putamen (P < 0.001); early l‐dopa–treated PD patients showed additional loss of [11C]IMA107 in the caudate (P < 0.001; annual decline 3.6%) and putamen (P < 0.001; annual decline 2.8%), but loss of [11C]PE2I only in the putamen (P < 0.001; annual decline 6.8%). Lower [11C]IMA107 correlated with lower [11C]PE2I in the caudate (rho = 0.51; P < 0.01) and putamen (rho = 0.53; P < 0.01). Longer disease duration correlated with lower [11C]IMA107 in the caudate (rho = –0.72; P < 0.001) and putamen (rho = –0.48; P < 0.01), and with lower [11C]PE2I only in the putamen (rho = –0.65; P < 0.001). Higher burden of motor symptoms correlated with lower [11C]IMA107 in the caudate (rho = –0.42; P < 0.05) and putamen (rho = –0.41; P < 0.05), and with lower [11C]PE2I only in the putamen (rho = –0.69; P < 0.001).ConclusionOur findings demonstrate loss of phosphodiesterase 10A levels very early in the course of PD and is associated with the gradual and progressive increase of motor symptoms. Phosphodiesterase 10A imaging shows similar potential with dopamine transporter imaging to follow disease progression.
Schubert JJ, Veronese M, Bodini B, et al., 2019, Dynamic PET with 11C-and 18F-tracers for measuring cerebrospinal fluid alterations in multiple sclerosis, 35th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS) / 24th Annual Conference of Rehabilitation in MS, Publisher: SAGE PUBLICATIONS LTD, Pages: 706-707, ISSN: 1352-4585
Roussakis A, Lao-Kaim N, Piccini P, 2019, Brain imaging and impulse control disorders in Parkinson’s disease, Current Neurology and Neuroscience Reports, Vol: 19, ISSN: 1528-4042
Purpose of reviewParkinson’s disease (PD) has a wide spectrum of symptoms including the presence of psychiatric disease. At present, most treatment plans, comprised of dopaminergic drugs, are chronic and complex. Though dopaminergic agents are quite efficient in managing the motor aspects of the disease, chronic pharmacotherapy specifically with dopamine receptor agonists has been highly linked to the occurrence of Impulse Compulsive disorder (ICD), which can be problematic for individual patients.Recent findingsMuch of what is known today about PD-related ICD stems from brain imaging studies, however, evidence is not quite conclusive. Research in the field has been focused on identifying the underlying mechanisms of PD-related ICD and understanding the functions of the structures involved in the reward network. SummaryThis article presents an update of recent findings from key neuroimaging studies in PD-related ICD, discusses results from controversial studies, and identifies areas for future research in the field.
Pagano G, Wilson H, Yousaf T, et al., 2019, Comparison of PDE10A and DAT expression as markers of disease burden in early Parkinson's disease, 5th Congress of the European-Academy-of-Neurology (EAN), Publisher: WILEY, Pages: 532-532, ISSN: 1351-5101
Lao-Kaim NP, Martin-Bastida A, Roussakis A-A, et al., 2019, Multimodal imaging of neuromelanin and dopamine transporters in Parkinson's disease reveals asymmetrical relationships within the nigrostriatal system, 5th Congress of the European-Academy-of-Neurology (EAN), Publisher: WILEY, Pages: 99-99, ISSN: 1351-5101
Hannaway N, Lao-Kaim NP, Martin-Bastida A, et al., 2019, Functional responses to joystick movements during Parkinson's disease progression: a longitudinal fMRI study, 5th Congress of the European-Academy-of-Neurology (EAN), Publisher: WILEY, Pages: 227-227, ISSN: 1351-5101
Martin Bastida A, Lao-Kaim N, Roussakis A, et al., 2019, Relationship between neuromelanin and dopamine terminals within the parkinson’s nigrostriatal system, Brain, Vol: 142, Pages: 2023-2036, ISSN: 1460-2156
Parkinson’s disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterising its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we utilised neuromelanin-sensitive magnetic resonance imaging and the highly specific dopamine transporter positron emission tomography radioligand, 11C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients with bilateral Parkinson’s disease. Fifteen healthy controls also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal/ventral tiers and striatal nuclei into pre/post-commissural sub-regions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation. In vivo, Parkinson’s disease subjects displayed reduced neuromelanin levels in the ventral (-30±28%) and dorsal tiers (-21±24%) as compared to the control group (F1,43 = 11.95, P = 0.001). Within the Parkinson’s disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier (F1,29 = 36.19, P < 0.001) and lower in the clinically-defined most affected side (F1,29 = 4.85, P = 0.036). Similarly, lower dopamine transporter density was observed in the ventral tier (F1,29 = 76.39, P < 0.001) and clinically-defined most affected side (F1,29 = 4.21, P = 0.049). Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-d
Roussakis A-A, Mohamed MA, Myers J, et al., 2019, Astrogliosis in Parkinson's disease dementia: a preliminary report with brain, 5th Congress of the European-Academy-of-Neurology (EAN)
Parker RA, TRANSEURO consortium, Piccini P, 2019, Designing stem-cell-based dopamine cell replacement trials for Parkinson's disease, Nature Medicine, Vol: 25, Pages: 1045-1053, ISSN: 1078-8956
Clinical studies of Parkinson’s disease (PD) using a dopamine cell replacment strategy have been tried for more than 30 years. The outcomes following transplantation of human fetal ventral mesencephalic tissue (hfVM) have been variable, with some patients coming off their anti-PD treatment for many years and others not responding and/or developing significant side effects, including graft-induced dyskinesia. This led to a re-appraisal of the best way to do such trials, which resulted in a new European-Union-funded allograft trial with fetal dopamine cells across several centers in Europe. This new trial, TRANSEURO (NCT01898390), is an open-label study in which some individuals in a large observational cohort of patients with mild PD who were undergoing identical assessments were randomly selected to receive transplants of hfVM. The TRANSEURO trial is currently ongoing as researchers have completed both recruitment into a large multicenter observational study of younger onset early-stage PD and transplantation of hfVM in 11 patients. While completion of TRANSEURO is not expected until 2021, we feel that sharing the rationale for the design of TRANSEURO, along with the lessons we have learned along the way, can help inform researchers and facilitate planning of transplants of dopamine-producing cells derived from human pluripotent stem cells for future clinical trials.
Roussakis A, Gennaro M, Lao-Kaim N, et al., 2019, Dopamine transporter density in de novo Parkinson’s disease does not relate to the development of levodopa-induced dyskinesias, Journal of Neuroinflammation and Neurodegenerative Diseases, Vol: 3
Background: In Parkinson’s disease (PD), the onset of levodopa-induced dyskinesias (LIDs) is difficult to predict. This study examines whether dopamine transporter (DAT)-specific SPECT imaging in de novo PD relates to later development of LIDs.Methods: 42 de novo unilateral PD participants received DAT-specific SPECT imaging with 123I-FP-CIT at time of diagnosis. At five years post-diagnosis, all PD patients were clinically evaluated and divided into two groups based on whether they had or had not developed LIDs. Fourteen gender- and age-matched healthy volunteers undertook 123I-FP-CIT SPECT imaging and were included as controls. A semi-quantification approach was used for the 123I-FP-CIT data using the occipital cortex as the reference region. We calculated specific binding ratios (SBR) for the caudate and putamen (posterior and anterior putaminal subregions). In parallel, we analysed our 123I-FP-CIT dataset with a voxel-based analysis approach.Results: PD patients had significantly lower striatal 123I-FP-CIT SBR values in comparison to controls (p<0.001). After five years, dyskinetic patients (N=10) were taking higher daily doses of dopaminergic medication (p<0.001) and had more severe disease (difference in Hoehn & Yahr staging scores p<0.05) as compared to the nondyskinetic group (N=32). At the time of diagnosis, 123I-FP-CIT SBR values were not statistically different between the two groups for all striatal regions (p>0.05). SPM voxel-based analysis did not show a statistically significant difference between the two groups (p>0.05).Conclusion: 123I-FP-CIT SPECT imaging, performed at diagnosis in de novo early-stage PD could not differentiate patients who will develop LIDs within five years from those who will not.
Reilmann R, Gordon MF, Anderson KE, et al., 2019, The Efficacy and Safety Results of Laquinimod as a Treatment for Huntington Disease (LEGATO-HD), 71st Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
Maxan A, Mason S, Saint-Pierre M, et al., 2018, Outcome of cell suspension allografts in a patient with Huntington's disease, Annals of Neurology, Vol: 84, Pages: 950-956, ISSN: 0364-5134
For patients with incurable neurodegenerative disorders such as Huntington's (HD) and Parkinson's disease, cell transplantation has been explored as a potential treatment option. Here, we present the first clinicopathological study of a patient with HD in receipt of cell-suspension striatal allografts who took part in the NEST-UK multicenter clinical transplantation trial. Using various immunohistochemical techniques, we found a discrepancy in the survival of grafted projection neurons with respect to grafted interneurons as well as major ongoing inflammatory and immune responses to the grafted tissue with evidence of mutant huntingtin aggregates within the transplant area. Our results indicate that grafts can survive more than a decade post-transplantation, but show compromised survival with inflammation and mutant protein being observed within the transplant site. Ann Neurol 2018; 1-7.
Martin-Bastida A, Lao-Kaim N, Pietracupa S, et al., 2018, Assessing working memory dysfunction with letter n-back functional MRI task in early-stage Parkinson's disease, International Congress of Parkinson's Disease and Movement Disorders, Publisher: WILEY, Pages: S688-S688, ISSN: 0885-3185
Martin-Bastida A, Lao-Kaim N, Pietracupa S, et al., 2018, Compensatory functional activations in early-stage Parkinson's disease: A cross-sectional motor planning fMRI study, International Congress of Parkinson's Disease and Movement Disorders, Publisher: WILEY, Pages: S653-S653, ISSN: 0885-3185
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