Andrew J Lees

University College London, Londinium, England, United Kingdom

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Publications (411)2512.88 Total impact

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    ABSTRACT: Background: It has been suggested that all patients with Parkinson's disease (PD) who undergo functional neurosurgery have difficulties in slowing down in high conflict tasks. However, it is unclear whether concomitant dopaminergic medication is responsible for this impairment. Objective: To assess perceptual decision making in PD patients with bilateral deep brain stimulation. Methods: We tested 27 PD patients with bilateral deep brain stimulation on a task in which participants had to filter task relevant information from background noise. Thirteen patients were treated with Levodopa monotherapy and 14 patients were treated with Levodopa in combination with a dopamine agonist. Results were compared to healthy matched controls. Results: We found that all PD patients who were treated with a dopamine agonist made faster decisions than controls and PD patients who were not exposed to a dopamine agonist. Further, all patients made more errors than controls, but there was no difference between the two patient groups. Conclusions: Our results suggest that dopamine agonist therapy rather than deep brain stimulation is likely responsible for the inability to slow down in high conflict situations in PD. These results further strengthen the need to reduce dopamine agonists in PD patients undergoing functional neurosurgery in order to prevent them making inadvisable decisions.
    Journal of Parkinson's disease. 07/2014;
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    ABSTRACT: Articles Davunetide in patients with progressive supranuclear palsy: a randomised, double-blind, placebo-controlled phase 2/3 trial Summary Background In preclinical studies, davunetide promoted microtubule stability and reduced tau phosphorylation. Because progressive supranuclear palsy (PSP) is linked to tau pathology, davunetide could be a treatment for PSP. We assessed the safety and effi cacy of davunetide in patients with PSP.
    The Lancet Neurology 07/2014; 13(7):676-685. · 23.92 Impact Factor
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    ABSTRACT: The aim of this study was to assess the neuropsychological behavior of Parkinson's disease (PD) patients with addictive behaviors. Characteristically, these patients have younger onset of PD, higher novelty-seeking personality traits, jump to conclusions, and often make irrational choices. We assessed whether PD patients with and without addictive behaviors have deficits in a sequential sampling task, often called the secretary problem. In this task, participants needed to pick the best out of multiple offers. Critically, once participants rejected a deal, this option became unavailable. Thus, decisions needed to be balanced not to stop too soon or sample for too long and miss the best deal. We tested 13 PD patients with and 13 patients without addictive behaviors. Results were compared to healthy volunteers. We found that all patients declined fewer options before committing to a deal. There was, however, no difference between the two patient groups. Furthermore, there was no difference in overall choice rank between patients and controls. These results suggest that, compared to controls, PD patients gather less evidence before committing to an offer, but have no deficits in recognizing the best deal out of many options, regardless of whether or not they have addictive behaviors.
    Movement Disorders Clinical Practice. 07/2014;
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    ABSTRACT: Clinical and neuropathological similarities between Dementia with Lewy Bodies (DLB), ParkinsonÕs and AlzheimerÕs diseases (PD and AD, respectively) suggest that these disorders may share etiology. To test this hypothesis we have performed an association study of 54 genomic regions, previously implicated in PD or AD, in a large cohort of DLB cases and controls. The cohort comprised 788 DLB cases and 2624 controls. To minimize the issue of potential misdiagnosis, we have also performed the analysis including only neuropathologically proven DLB cases (667 cases). Results show that the APOE is a strong genetic risk factor for DLB, confirming previous findings, and that the SNCA and SCARB2 loci are also associated after study-wise Bonferroni correction, although these have a different association profile than the associations reported for the same loci in PD. We have previously shown that the p.N370S variant in GBA is associated with DLB, which, together with the findings at the SCARB2 locus, suggests a role for lysosomal dysfunction in this disease. These results indicate that DLB has a unique genetic risk profile when compared to the two most common neurodegenerative diseases and that the lysosome may play an important role in the etiology of this disorder. We make all these data available.
    Human Molecular Genetics 06/2014; · 7.69 Impact Factor
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    ABSTRACT: Mutations in the vacuolar protein sorting 35 homolog (VPS35) gene at the PARK17 locus, encoding a key component of the retromer complex, were recently identified as a new cause of late-onset, autosomal dominant Parkinson's disease (PD). Here we explore the pathogenic consequences of PD-associated mutations in VPS35 using a number of model systems. VPS35 exhibits a broad neuronal distribution throughout the rodent brain, including within the nigrostriatal dopaminergic pathway. In the human brain, VPS35 protein levels and distribution are similar in tissues from control and PD subjects, and VPS35 is not associated with Lewy body pathology. The common D620N missense mutation in VPS35 does not compromise its protein stability or localization to endosomal and lysosomal vesicles, or the vesicular sorting of the retromer cargo, sortilin, SorLA and cation-independent mannose 6-phosphate receptor, in rodent primary neurons or patient-derived human fibroblasts. In yeast we show that PD-linked VPS35 mutations are functional and can normally complement VPS35 null phenotypes suggesting that they do not result in a loss-of-function. In rat primary cortical cultures the overexpression of human VPS35 induces neuronal cell death and increases neuronal vulnerability to PD-relevant cellular stress. In a novel viral-mediated gene transfer rat model, the expression of D620N VPS35 induces the marked degeneration of substantia nigra dopaminergic neurons and axonal pathology, a cardinal pathological hallmark of PD. Collectively, these studies establish that dominant VPS35 mutations lead to neurodegeneration in PD consistent with a gain-of-function mechanism, and support a key role for VPS35 in the development of PD.
    Human Molecular Genetics 04/2014; · 7.69 Impact Factor
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    ABSTRACT: Parkinsonian diseases comprise a heterogeneous group of neurodegenerative disorders, which show significant clinical and pathological overlap. Accurate diagnosis still largely relies on clinical acumen; pathological diagnosis remains the gold standard. There is an urgent need for biomarkers to diagnose parkinsonian disorders, particularly in the early stages when diagnosis is most difficult. In this review, several of the most promising cerebrospinal fluid candidate markers will be discussed. Their strengths and limitations will be considered together with future developments in the field.
    Journal of neurology, neurosurgery, and psychiatry 04/2014; · 4.87 Impact Factor
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    ABSTRACT: Cognitive impairment (CI) is an exclusion criterion for the diagnosis of multiple system atrophy (MSA), according to the second consensus statement. This view was recently challenged by patients with pathologically confirmed MSA who were reported to have dementia. With an aim to investigate the pathological substrate of CI in MSA, quantitative assessment of the glial and neuronal cytoplasmic inclusions and semiquantitative assessment of neuronal loss in the cortical and limbic regions was performed. No differences in the severity of these MSA-related pathological findings were identified between nine MSA cases with CI and nine MSA cases with normal cognition. Alzheimer's-related pathological changes, cerebral amyloid angiopathy, and cerebrovascular disease did not differ between the two MSA groups. MSA-specific α-synuclein and secondary pathological conditions were not more severe in MSA cases with CI, suggesting that although CI may be intrinsic to the MSA disease process, further investigation into the pathological basis of cognitive impairment in MSA is warranted. © 2014 International Parkinson and Movement Disorder Society
    Movement Disorders 04/2014; · 5.63 Impact Factor
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    ABSTRACT: Background: Data from an open label randomised controlled trial have suggested possible advantages on both motor and non-motor measures in patients with Parkinson's disease following 12 months exposure to exenatide. Objective: Continued follow up of these same patients was performed to investigate whether these possible advantages persisted in the prolonged absence of this medication. Methods: All participants from an open label, randomised controlled trial of exenatide as a treatment for Parkinson's disease, were invited for a further follow up assessment at the UCL Institute of Neurology. This visit included all 20 individuals who had previously completed twelve months exposure to exenatide 10ug bd and the 24 individuals who had acted as randomised controls. Motor severity of PD was compared after overnight withdrawal of conventional PD medication using blinded video assessment of the MDS-UPDRS, together with several non-motor tests. This assessment was thus 24 months after their original baseline visit, i.e. 12 months after cessation of exenatide. Results: Compared to the control group of patients, patients previously exposed to exenatide had an advantage of 5.6 points (95% CI, 2.2-9.0; p = 0.002) using blinded video rating of the MDS-UPDRS part 3 motor subscale. There was also a difference of 5.3 points; (95% CI, 9.3-1.4; p = 0.006) between the 2 groups on the Mattis Dementia Rating scale. Conclusions: While these data must still not be interpreted as evidence of neuroprotection, they nevertheless provide strong encouragement for the further study of this drug as a potential disease modifying agent in Parkinson's disease.
    Journal of Parkinson's disease. 03/2014;
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    ABSTRACT: The use of telemedicine is becoming increasingly popular in assisting with the home management of People with Dementia (PwD) by offering services to the carers that may enhance their ability to care for their relative for longer. A computerized platform, ALADDIN, was evaluated in its usefulness to reduce carer burden and distress and to improve their quality of life, in an attempt to delay institutionalization of PwD. ALADDIN offers educational material about dementia to carers and provides the opportunity to contact other carers and clinicians. ALADDIN also facilitates remote monitoring of the PwD and their carers by the clinicians to enable speedy delivery of appropriate intervention. The ALADDIN platform was piloted at three European sites, and used by thirty carers of PwD living in the community (platform group). The platform group and a control group of thirty PwD and their carers were assessed at baseline, 3 months, and 6 months. The results showed a significant improvement in the quality of life of the carers in the platform group, with some reduction in carer burden and distress. The platform was useful in monitoring the patients and facilitating contact with other professionals. Access to and use of the ALADDIN platform was rated positively by carers and clinicians. The ALADDIN platform's usefulness and applicability for prolonging the home management of PwD are discussed.
    Journal of Alzheimer's disease: JAD 03/2014; · 4.17 Impact Factor
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    ABSTRACT: Parkinson's disease (PD) and osteoporosis are chronic diseases associated with increasing age. Single studies have reported associations between them and the major consequence, namely, increased risk of fractures. The aim of this systematic review and meta-analysis was to evaluate the relationship of PD with osteoporosis, bone mineral density (BMD) and fracture risk. A literature search was undertaken on 4 September 2012 using multiple indexing databases and relevant search terms. Articles were screened for suitability and data extracted where studies met inclusion criteria and were of sufficient quality. Data were combined using standard meta-analysis methods. 23 studies were used in the final analysis. PD patients were at higher risk of osteoporosis (OR 2.61; 95% CI 1.69 to 4.03) compared with healthy controls. Male patients had a lower risk for osteoporosis and osteopenia than female patients (OR 0.45; 95% CI 0.29 to 0.68). PD patients had lower hip, lumbar spine and femoral neck BMD levels compared with healthy controls; mean difference, -0.08, 95% CI -0.13 to -0.02 for femoral neck; -0.09, 95% CI -0.15 to -0.03 for lumbar spine; and -0.05, 95% CI -0.07 to -0.03 for total hip. PD patients were also at increased risk of fractures (OR 2.28; 95% CI 1.83 to 2.83). This systematic review and meta-analysis demonstrate that PD patients are at higher risk for both osteoporosis and osteopenia compared with healthy controls, and that female patients are at greater risk than male patients. Patients with PD also have lower BMD and are at increased risk of fractures.
    Journal of neurology, neurosurgery, and psychiatry 03/2014; · 4.87 Impact Factor
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    ABSTRACT: Multiple system atrophy (MSA) is a progressive neurodegenerative disease presenting clinically with parkinsonian, cerebellar, and autonomic features. α-Synuclein (αsyn), encoded by the gene SNCA, is the main constituent of glial cytoplasmic inclusion (GCI) found in oligodendrocytes in MSA, but the methods of its accumulation have not been established. The aim of this study is to investigate alterations in regional and cellular SNCA mRNA expression in MSA as a possible substrate for GCI formation. Quantitative reverse transcription polymerase chain reaction (qPCR) was performed on postmortem brain samples from 15 MSA, 5 IPD, and 5 control cases to investigate regional expression in the frontal and occipital regions, dorsal putamen, pontine base, and cerebellum. For cellular expression analysis, neurons and oligodendrocytes were isolated by laser-capture microdissection from five MSA and five control cases. SNCA mRNA expression was not significantly different between the MSA, IPD and control cases in all regions (multilevel model, P = 0.14). After adjusting for group effect, the highest expression was found in the occipital cortex while the lowest was in the putamen (multilevel model, P < 0.0001). At the cellular level, MSA oligodendrocytes expressed more SNCA than control oligodendrocytes and expression in MSA neurons was slightly lower than that in controls, however, these results did not reach statistical significance. We have demonstrated regional variations in SNCA expression, which is higher in cortical than subcortical regions. This study is the first to demonstrate SNCA mRNA expression by oligodendrocytes in human postmortem tissue using qPCR and, although not statistically significant, could suggest that this may be increased in MSA compared to controls. GLIA 2014.
    Glia 03/2014; · 5.07 Impact Factor
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    ABSTRACT: We report the case of a 75-year-old ex-professional boxer who developed diplopia and eye movement abnormalities in his 60's followed by memory impairment, low mood and recurrent falls. Examination shortly before death revealed hypomimia, dysarthria, vertical supranuclear gaze palsy and impaired postural reflexes. Pathological examination demonstrated 4-repeat tau neuronal and glial lesions, including tufted astrocytes, consistent with a diagnosis of progressive supranuclear palsy. In addition, neurofibrillary tangles composed of mixed 3-repeat and 4-repeat tau and astrocytic tangles in a distribution highly suggestive of chronic traumatic encephalopathy were observed together with limbic TDP-43 pathology. Possible mechanisms for the co-occurrence of these two tau pathologies are discussed.
    Acta neuropathologica communications. 02/2014; 2(1):24.
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    ABSTRACT: It is believed that glycogen synthase kinase-3 (GSK-3) hyperphosphorylates tau protein in progressive supranuclear palsy (PSP). The Tau Restoration on PSP (TAUROS) study was a double-blind, placebo-controlled, randomized trial to assess the efficacy, safety, and tolerability of tideglusib, a GSK-3 inhibitor, as potential treatment for PSP. The study enrolled 146 PSP patients with mild-to-moderate disease who were randomized to receive once-daily 600 mg tideglusib, 800 mg tideglusib, or placebo (ratio, 2:2:1) administered orally over 52 weeks. The primary endpoint was the change from baseline to week 52 on the PSP rating scale. Secondary endpoints were safety and tolerability of tideglusib, changes in motor function (the Timed Up and Go Test), cognition (Dementia Rating Scale-2, Frontal Assessment Battery, verbal fluency), apathy (Starkstein scale), activities of daily living (Schwab and England scale; Unified Parkinson's Disease Rating Scale, part II), quality of life (EuroQol), and Global Clinical Assessment. Brain atrophy on magnetic resonance imaging and several biomarkers in plasma and cerebrospinal fluid also were examined. No significant differences were detected in the primary or secondary endpoints at week 52 between placebo and either dose of tideglusib. Tideglusib was safe, with the exception of some asymptomatic, transient, and reversible transaminase elevations (mainly alanine aminotransferase) in 9% of patients, and diarrhea in 13% of patients. Tideglusib was generally well tolerated but it did not show clinical efficacy in patients with mild-to-moderate PSP. © 2014 International Parkinson and Movement Disorder Society.
    Movement Disorders 02/2014; · 5.63 Impact Factor
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    ABSTRACT: The aim of the study was to develop a culturally adapted translation of the 12-item smell identification test from Sniffin’ Sticks (SS-12) for the Estonian population in order to help diagnose Parkinson’s disease (PD). Methods A standard translation of the SS-12 was created and 150 healthy Estonians were questioned about the smells used as response options in the test. Unfamiliar smells were replaced by culturally familiar options. The adapted SS-12 was applied to 70 controls in all age groups, and thereafter to 50 PD patients and 50 age- and sex-matched controls. Results 14 response options from 48 used in the SS-12 were replaced with familiar smells in an adapted version, in which the mean rate of correct response was 87% (range 73 to 99) compared to 83% with the literal translation (range 50 to 98). In PD patients, the average adapted SS-12 score (5.4/12) was significantly lower than in controls (average score 8.9/12), p <0.0001. A multiple linear regression using the score in the SS-12 as the outcome measure showed that diagnosis and age independently influenced the result of the SS-12. A logistic regression using the SS12 and age as covariates showed that the SS12 (but not age) correctly classified 79.0% of subjects into the PD and control category, using a cut-off of <7 gave a sensitivity of 76% and specificity of 86% for the diagnosis of PD. Conclusions The developed SS-12 cultural adaption is appropriate for testing olfaction in Estonia for the purpose of PD diagnosis.
    Parkinsonism & Related Disorders 01/2014; · 3.27 Impact Factor
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    ABSTRACT: The aim of this observational study was to investigate the safety and efficacy of tolcapone under practice conditions. This 12-month non-interventional study was conducted from November 2005 to August 2009. Safety parameters were incidence of adverse drug reactions (ADRs), signs and symptoms of liver failure, and liver monitoring. Efficacy was evaluated on the basis of the assessment by physicians and patients by means of the clinical global impression scale. Data from 391 patients were available for evaluation. Fifty-six ADRs were documented in 45 patients: most frequently, increase in liver enzymes (5.6%), diarrhea (2.6%), and nausea (1.3%). No serious ADRs or fulminant hepatotoxicity occurred. Sixteen patients discontinued the treatment with tolcapone because of adverse events, thereof 7 because of increase in liver enzymes, as prespecified in the protocol. Sixty-two elevations of aspartate aminotransferase or alanine aminotransferase occurred in 34 patients (8.7%), most of them within the first 3 months after initiating tolcapone. Five patients (1.3%) experienced clinically relevant elevations (>2xULN). In most patients with minimally elevated transaminase levels, tolcapone was continued, leading to normalization of transaminase levels in 74% of these patients. Two patients died but without causal relationship to tolcapone. The physicians reported improvement of clinical global impression for 71.7% of the patients after 3 months and for 59.1% of the patients after 12 months. Under routine practice conditions, tolcapone was shown to be safe and effective in patients with Parkinson disease. Significant liver transaminase elevations were rare and generally returned to normal without intervention in most patients. This study confirms the low risk for hepatotoxicity associated with tolcapone.
    Clinical neuropharmacology 01/2014; 37(1):1-5. · 2.35 Impact Factor
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    ABSTRACT: Background Problematic Internet Use (PIU) have been associated with impulse control disorders (ICD), and postulated to share characteristics of a behavioural addiction with both impulsive and compulsive features. However, Internet use has not been previously systematically studied in Parkinson’s disease. Aim We explore Internet use in PD patients with and without ICDs and matched healthy controls. We hypothesise that the PD-ICD patients will spend more time on the Internet, accessing websites related to their ICDs, compared with PD patients without ICDs and healthy volunteers. Methods Our study is the first to systematically explore problematic Internet use in patients with PD, with and without ICDs. Twenty-nine PD patients with ICDs, twenty PD patients without ICDs and nineteen healthy controls were recruited. All participants endorsed using the Internet for non-essential purposes. They underwent a semi-structured interview and completed questionnaires including the Yale-Brown Obsessive Compulsive Scale adapted for Internet use (Y-BOCS-Internet). Results PD-ICD patients scored significantly higher on the Y-BOCS-Internet than the PD-control and HV groups (PD-ICD: 13.69; PD-control: 5.42; HV: 4.70; p<0.0001). Compared to PD controls and HV groups, the PD-ICD group spent more time on the Internet (p=0.0001), described significantly more effort to resist Internet use (p=0.0002), thoughts about Internet use (p<0.0001) and its interference with their life functioning (p=0.0025). Discussion Our results suggest that PD patients with ICDs have a relative increased tendency towards excessive Internet use compared to those without ICDs and healthy controls. Clinicians should actively screen for excessive Internet use in patients with ICDs.
    Parkinsonism & Related Disorders 01/2014; · 3.27 Impact Factor
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    ABSTRACT: Progressive supranuclear palsy is a rare parkinsonian disorder with characteristic neurofibrillary pathology consisting of hyperphosphorylated tau protein. Common variation defining the microtubule associated protein tau gene (MAPT) H1 haplotype strongly contributes to disease risk. A recent genome-wide association study (GWAS) revealed 3 novel risk loci on chromosomes 1, 2, and 3 that primarily implicate STX6, EIF2AK3, and MOBP, respectively. Genetic associations, however, rarely lead to direct identification of the relevant functional allele. More often, they are in linkage disequilibrium with the causative polymorphism(s) that could be a coding change or affect gene expression regulatory motifs. To identify any such changes, we sequenced all coding exons of those genes directly implicated by the associations in progressive supranuclear palsy cases and analyzed regional gene expression data from control brains to identify expression quantitative trait loci within 1 Mb of the risk loci. Although we did not find any coding variants underlying the associations, GWAS-associated single-nucleotide polymorphisms at these loci are in complete linkage disequilibrium with haplotypes that completely overlap with the respective genes. Although implication of EIF2AK3 and MOBP could not be fully assessed, we show that the GWAS single-nucleotide polymorphism rs1411478 (STX6) is a strong expression quantitative trait locus with significantly lower expression of STX6 in white matter in carriers of the risk allele.
    Neurobiology of Aging. 01/2014; 35(6):1514.e1–1514.e12.
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    ABSTRACT: The Bradykinesia Akinesia Incoordination (BRAIN) test is a computer keyboard-tapping task that was developed for use in assessing the effect of symptomatic treatment on motor function in Parkinson's disease (PD). An online version has now been designed for use in a wider clinical context and the research setting. Validation of the online BRAIN test was undertaken in 58 patients with Parkinson's disease (PD) and 93 age-matched, non-neurological controls. Kinesia scores (KS30, number of key taps in 30 seconds), akinesia times (AT30, mean dwell time on each key in milliseconds), incoordination scores (IS30, variance of travelling time between key presses) and dysmetria scores (DS30, accuracy of key presses) were compared between groups. These parameters were correlated against total motor scores and sub-scores from the Unified Parkinson's Disease Rating Scale (UPDRS). Mean KS30, AT30 and IS30 were significantly different between PD patients and controls (p≤0.0001). Sensitivity for 85% specificity was 50% for KS30, 40% for AT30 and 29% for IS30. KS30, AT30 and IS30 correlated significantly with UPDRS total motor scores (r = -0.53, r = 0.27 and r = 0.28 respectively) and motor UPDRS sub-scores. The reliability of KS30, AT30 and DS30 was good on repeated testing. The BRAIN test is a reliable, convenient test of upper limb motor function that can be used routinely in the outpatient clinic, at home and in clinical trials. In addition, it can be used as an objective longitudinal measurement of emerging motor dysfunction for the prediction of PD in at-risk cohorts.
    PLoS ONE 01/2014; 9(4):e96260. · 3.73 Impact Factor

Publication Stats

16k Citations
2,512.88 Total Impact Points


  • 2002–2014
    • University College London
      • • Institute of Neurology
      • • Department of Molecular Neuroscience
      • • Department of Neuroinflammation
      Londinium, England, United Kingdom
    • UCL Eastman Dental Institute
      Londinium, England, United Kingdom
    • Academisch Medisch Centrum Universiteit van Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 1998–2014
    • University of London
      Londinium, England, United Kingdom
  • 2013
    • Centro de Investigación Biomédica en Red, Enfermedades Neurodegenerativas
      Madrid, Madrid, Spain
    • King's College London
      • Department of Psychological Medicine
      London, ENG, United Kingdom
  • 2012–2013
    • Universidade Federal do Paraná
      • Hospital de Clínicas
      Curitiba, Estado do Parana, Brazil
    • University of Campinas
      Conceição de Campinas, São Paulo, Brazil
    • Sanford Research
      Sioux Falls, South Dakota, United States
    • Birkbeck, University of London
      • Department of Psychological Sciences
      London, ENG, United Kingdom
    • Universitário de Belo Horizonte - UNI-BH
      Cidade de Minas, Minas Gerais, Brazil
    • Medizinische Universität Innsbruck
      • Univ.-Klinik für Neurologie
      Innsbruck, Tyrol, Austria
    • University of Thessaly
      • Κλινική Νευρολογίας
      Iolcus, Thessaly, Greece
    • Instituto Nacional de Neurología y Neurocirugía
      Tlalpam, The Federal District, Mexico
  • 2006–2013
    • Federal University of Minas Gerais
      • • Faculty of Medicine
      • • Hospital das Clínicas
      Belo Horizonte, Estado de Minas Gerais, Brazil
    • Dharwad Institute of Mental Health and Neurosciences
      Hubli, Karnātaka, India
    • Radboud University Nijmegen
      • Department of Neurology
      Nijmegen, Provincie Gelderland, Netherlands
  • 2002–2013
    • Imperial College London
      • • Division of Brain Sciences
      • • Faculty of Medicine
      London, ENG, United Kingdom
  • 1999–2012
    • Queen Mary, University of London
      • The Blizard Institute of Cell and Molecular Science
      Londinium, England, United Kingdom
  • 2011
    • Hospital São Rafael
      Bahia, Estado de Bahía, Brazil
    • Wellcome Trust
      Londinium, England, United Kingdom
    • The National Institute of Neurology and Neurosurgery
      Tlalpam, The Federal District, Mexico
  • 2010
    • Royal Melbourne Hospital
      Melbourne, Victoria, Australia
    • Nottingham University Hospitals NHS Trust
      • Department of Clinical Psychology and Neuropsychology
      Nottigham, England, United Kingdom
  • 2009
    • The University of Manchester
      • School of Translational Medicine
      Manchester, ENG, United Kingdom
    • National Institute on Aging
      • Laboratory of Neurogenetics (LNG)
      Baltimore, Maryland, United States
  • 2007–2009
    • Monash University (Australia)
      • Van Cleef/Roet Centre for Nervous Diseases, and Department of Neuroscience
      Melbourne, Victoria, Australia
  • 2008
    • National Institutes of Health
      • Laboratory of Neurogenetics
      Bethesda, MD, United States
    • Haukeland University Hospital
      Bergen, Hordaland, Norway
    • Medical University of Vienna
      Wien, Vienna, Austria
  • 2005–2008
    • SAE Institute, London
      Oxford, England, United Kingdom
    • Nottinghamshire Healthcare NHS Trust
      Nottigham, England, United Kingdom
    • Centre Hospitalier de Valenciennes
      Valenciennes, Nord-Pas-de-Calais, France
  • 2002–2008
    • Newcastle University
      • Institute for Ageing and Health
      Newcastle upon Tyne, ENG, United Kingdom
  • 2002–2005
    • WWF United Kingdom
      Londinium, England, United Kingdom
  • 2003
    • MRC Cognition and Brain Sciences Unit
      Cambridge, England, United Kingdom
    • Sapienza University of Rome
      • Department of Anatomical, Histological, Forensic Medicine and Orthopedic Science
      Roma, Latium, Italy
  • 1999–2002
    • University Hospital Center Pointe-à-Pitre
      La Pointe à Pitre, Guadeloupe, Guadeloupe