Dag Aarsland

Karolinska Institutet, Solna, Stockholm, Sweden

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Publications (325)1766.91 Total impact

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    ABSTRACT: Alzheimer disease (AD) and Parkinson disease (PD) are the most common neurodegenerative disorders. For both diseases, early intervention is thought to be essential to the success of disease-modifying treatments. Cerebrospinal fluid (CSF) can reflect some of the pathophysiological changes that occur in the brain, and the number of CSF biomarkers under investigation in neurodegenerative conditions has grown rapidly in the past 20 years. In AD, CSF biomarkers are increasingly being used in clinical practice, and have been incorporated into the majority of clinical trials to demonstrate target engagement, to enrich or stratify patient groups, and to find evidence of disease modification. In PD, CSF biomarkers have not yet reached the clinic, but are being studied in patients with parkinsonism, and are being used in clinical trials either to monitor progression or to demonstrate target engagement and downstream effects of drugs. CSF biomarkers might also serve as surrogate markers of clinical benefit after a specific therapeutic intervention, although additional data are required. It is anticipated that CSF biomarkers will have an important role in trials aimed at disease modification in the near future. In this Review, we provide an overview of CSF biomarkers in AD and PD, and discuss their role in clinical trials.
    Nature Reviews Neurology 12/2014; · 15.52 Impact Factor
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    ABSTRACT: Neuropsychiatric symptoms in Alzheimer disease (AD) cause significant distress and present a complex clinical challenge for treatment. Pharmacological treatment options are limited to antipsychotics, which carry extensive safety issues. There is emerging evidence to support the potential benefits of memantine, currently licensed for moderate to severe AD, in the prophylaxis of neuropsychiatric symptoms. The MAIN-AD study is a double-blind randomized placebo-controlled withdrawal trial comparing memantine with antipsychotics for the treatment of neuropsychiatric symptoms over 24 weeks. A total of 199 people with probable AD living in care homes already receiving an antipsychotic were randomized to receive either memantine or to continue an antipsychotic. The primary outcomes were function (Bristol Activities of Daily Living Scale [BADLS]) and agitation (Cohen-Mansfield Agitation Inventory [CMAI]). Secondary outcomes were Neuropsychiatric Inventory (NPI), Mini-Mental State Examination (MMSE), and mortality. There was no significant difference between groups on the BADLS or CMAI. At 24 weeks, there was a nonsignificant adjusted difference in favor of memantine on the BADLS of 0.23 (95% CI -1.80-2.27; P = .82) and in favor of antipsychotic on the CMAI of 0.09 (95% CI -0.35-8.53; P = .07). Although there were no significant differences in total NPI, there were 5.01 (95% CI -1.68-11.70; P = .05) and 3.63 (95% CI -1.40-8.67; P = .16) point advantages favoring antipsychotics at weeks 12 and 24, respectively. In addition, in an exploratory analysis, individuals allocated to antipsychotics were significantly less likely to experience relapse of neuropsychiatric symptoms at all time points. The group receiving memantine had a nonsignificant 1.3-point advantage on the MMSE at 24 weeks. This study indicates no benefits for memantine in the long-term treatment and prophylaxis of clinically significant neuropsychiatric symptoms. The results did indicate some benefits for antipsychotic medications in reducing the relapse of neuropsychiatric symptoms, but this must be balanced against increased mortality risk. Copyright © 2014 AMDA – The Society for Post-Acute and Long-Term Care Medicine. Published by Elsevier Inc. All rights reserved.
    Journal of the American Medical Directors Association. 12/2014;
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    Non-Motor Dysfunctions in Parkinson's Disease and Related Disorders, Nice, France; 12/2014
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    ABSTRACT: Objectives: To find the frequency of probable REM sleep behavior disorder (RBD) in mild dementia with Lewybodies (DLB) as compared with mild Alzheimer’s dementia (AD). Method: A well validated sleep questionnaire, The Mayo Sleep Questionnaire (MSQ), was administered to the bed partners and caregivers of patients included in the dementia study of western Norway (Dem-West-study). The questionnaire includes screening questions to detect REM sleep behavior disorder (RBD) and other sleep disturbances. DLB was diagnosed according to the revised consensus criteria which includes RBD as a diagnostic criterion for DLB. Results: A total of 83 (37, 6%) persons were diagnosed with DLB and 138 (62.4%) persons were diagnosed with AD and were included in this study. Mean age in DLB was 77.0 years (7.2) and in AD 75.5 years (7.8), p=0.260 and mean MMSE scores were 23.0 (3.2) in DLB and 23.8 (2.2) in AD, p=0.028. Sleep partners confirmed probable RBD in 40 % of participants diagnosed with DLB and in 9 % of participants diagnosed with AD. The average duration of RBD symptoms among participants diagnosed with DLB was 6.2 years (SD=7.7) and 4.6 years (SD=4.0) in AD, p=0.583. Two DLB patients and three bed partners were seriously injured under RBD episodes. Twenty patients reported vivid or violent dreams: 16 (55.2%) with DLB and 4 (22.2%) with AD and, p=0.066. Conclusion: Probable RBD is frequently reported from bed partners of persons diagnosed clinically with mild DLB applying the MAYO sleep questionnaire (MSQ). Probable RBD was also reported in persons diagnosed clinically with AD. Probable RBD is potentially harmful for patients and bed partners in mild dementia. Circularity must be considered in this study as RBD was also part of the diagnostic criteria for DLB.
    Non-Motor Dysfunctions in Parkinson's Disease and Related Disorders, Niece, France; 12/2014
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    ABSTRACT: Cognitive impairment is one of the earliest, most common, and most disabling non-motor symptoms in Parkinson's disease (PD). Thus, routine screening of global cognitive abilities is important for the optimal management of PD patients. Few global cognitive screening instruments have been developed for or validated in PD patients. The Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and Dementia Rating Scale-2 (DRS-2) have been used extensively for cognitive screening in both clinical and research settings. Determining how to convert the scores between instruments would facilitate the longitudinal assessment of cognition in clinical settings and the comparison and synthesis of cognitive data in multicenter and longitudinal cohort studies. The primary aim of this study was to apply a simple and reliable algorithm for the conversion of MoCA to MMSE scores in PD patients. A secondary aim was to apply this algorithm for the conversion of DRS-2 to both MMSE and MoCA scores. The cognitive performance of a convenience sample of 360 patients with idiopathic PD was assessed by at least two of these cognitive screening instruments. We then developed conversion scores between the MMSE, MoCA, and DRS-2 using equipercentile equating and log-linear smoothing. The conversion score tables reported here enable direct and easy comparison of three routinely used cognitive screening assessments in PD patients. © 2014 International Parkinson and Movement Disorder Society
    Movement Disorders 11/2014; · 5.63 Impact Factor
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    ABSTRACT: Cognitive impairment in Parkinson's disease (PD) is common and does directly impact patients' everyday functioning. However, the underlying mechanisms of early cognitive decline are not known. This study explored the association between striatal dopaminergic deficits and cognitive impairment within a large cohort of early, drug-naïve PD patients and tested the hypothesis that executive dysfunction in PD is associated with striatal dopaminergic depletion. A cross-sectional multicenter cohort of 339 PD patients and 158 healthy controls from the Parkinson's Progression Markers Initiative study was analyzed. Each individual underwent cerebral single-photon emission CT (SPECT) and a standardized neuropsychological assessment with tests of memory as well as visuospatial and executive function. SPECT imaging was performed with [123I]FP-CIT, and specific binding ratios in left and right putamen and caudate nucleus were calculated. The association between specific binding ratios, cognitive domain scores, and age was analyzed using Pearson's correlations, partial correlation, and conditional process analysis. A small, but significant, positive association between total striatal dopamine transporter binding and the attention/executive domain was found (r = 0.141; P = 0.009) in PD, but this was not significant after adjusting for age. However, in a moderated mediation model, we found that cognitive executive differences between controls and patients with PD were mediated by an age-moderated striatal dopaminergic deficit. Our findings support the hypothesis that nigrostriatal dopaminergic deficit is associated with executive impairment, but not to memory or visuospatial impairment, in early PD. © 2014 International Parkinson and Movement Disorder Society
    Movement Disorders 10/2014; · 5.63 Impact Factor
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    ABSTRACT: Objective To test the hypothesis that depressive symptoms correlate with Alzheimer's disease (AD) type changes in CSF and structural and functional imaging including hippocampus volume, cortical thickness, white matter lesions, Diffusion tensor imaging (DTI), and fluoro-deoxy-glucose positron emission tomography (FDG-PET) in patient with subjective (SCI) and mild (MCI) cognitive impairment.Method In 60 patients, depressive symptoms were assessed using the Geriatric Depression Scale. The subjects underwent MRI, 18F-FDG PET imaging, and lumbar CSF extraction.ResultsSubjects with depressive symptoms (n = 24) did not have more pathological AD biomarkers than non-depressed. Uncorrected there were trends towards larger hippocampal volumes (P = 0.06), less orbital WM damage measured by DTI (P = 0.10), and higher orbital glucose metabolism (P = 0.02) in the depressed group. The findings were similar when SCI and MCI were analyzed separately. Similarly, in patients with pathological CSF biomarkers (i.e., predementia AD, n = 24), we found that correlations between scores on GDS and CSF Aß42 and P-tau indicated less severe AD-specific CSF changes with increasing depression.Conclusion Depressive symptoms are common in SCI/MCI, but are not associated with pathological imaging or CSF biomarkers of AD. Depression can explain cognitive impairment in SCI/MCI or add to cognitive impairment leading to an earlier clinical investigation in predementia AD.
    Acta Psychiatrica Scandinavica 10/2014; · 4.86 Impact Factor
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    ABSTRACT: Introduction: The aim of this review was to investigate whether there is a faster cognitive decline in dementia with Lewy bodies (DLB) than in Alzheimer's disease (AD) over time. Methods: PsycINFO and Medline were searched from 1946 to February 2013. A quality rating from 1 to 15 (best) was applied to the included studies. A quantitative meta-analysis was done on studies with mini mental state examination (MMSE) as the outcome measure. Results: A total of 18 studies were included. Of these, six (36%) reported significant differences in the rate of cognitive decline. Three studies reported a faster cognitive decline on MMSE in patients with mixed DLB and AD compared to pure forms, whereas two studies reported a faster decline on delayed recall and recognition in AD and one in DLB on verbal fluency. Mean quality scores for studies that did or did not differ were not significantly different. Six studies reported MMSE scores and were included in the meta-analysis, which showed no significant difference in annual decline on MMSE between DLB (mean 3.4) and AD (mean 3.3). Conclusions: Our findings do not support the hypothesis of a faster rate of cognitive decline in DLB compared to AD. Future studies should apply recent diagnostic criteria, as well as extensive diagnostic evaluation and ideally autopsy diagnosis. Studies with large enough samples, detailed cognitive tests, at least two years follow up and multivariate statistical analysis are also needed.
    Alzheimer's Research and Therapy 09/2014; · 3.50 Impact Factor
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    ABSTRACT: Dementia is characterized by a progressive cognitive decline and neuropsychiatric symptoms (NPSD) such as agitation, apathy and sleeping problems. There is some evidence of activation of inflammatory pathways in the brain in dementia, but little research has been performed regarding the role of neuroinflammation in NPSD, which might represent a potential novel target for treatment. The aim of this study was to examine the possible association between NPSD and cerebrospinal fluid (CSF) levels of the cytokines IL-6, TNF-α and IL-10, and the cytokine receptor sIL-1RII, in patients with dementia and NPSD. Ninety-four patients (mean age 79±8; 67% female) with a score on the Neuropsychiatric Inventory (NPI) ≥ 10 points, were included. Clinical assessment included administration of NPI, the Mini-Mental State Examination (MMSE) and the Cohen-Mansfield Agitation Inventory (CMAI). The cytokine levels in CSF samples were analysed by enzyme-linked immunosorbent assay. Correlations were statistically examined using Spearman's rank correlation coefficient (r), and simple- and multiple linear regression. The anti-inflammatory cytokine IL-10 showed reverse correlations with total NPI score (NPI-total=-0.001, t(90)= 8.50, p=0.004) and NPI sub-items agitation (Agitation=-0.007, t(90)=7.02, p=0.009) and night-time behaviour (Night time behaviour=-0.006, t(90)=6.34, p=0.01). There was a trend towards correlation between IL-10 and depression (Depression=-0.004, t(90)=2.96, p=0.09). Also, the soluble cytokine receptor sIL-1RII showed a trend towards correlation with apathy (Apathy=0.82, t(82)=3.62, p=0.06). The levels of IL-6 showed no significant correlations with NPSD. Levels of TNF-α were non-detectable. In Alzheimer's disease (AD) subjects (n=33), IL-6 showed reverse correlation with anxiety (r=-0.35, p=0.049). In mixed AD subjects (n=26), IL-10 showed reverse correlations with the total NPI score (r=-0.46, p=0.02) and depression (r=-0.45, p=0.02). The findings indicate a relationship between neuroinflammation and neuropsychiatric symptoms in AD in which anti-inflammatory signalling by IL-10 is beneficial from a mental health perspective.
    Brain Research Bulletin 09/2014; · 2.97 Impact Factor
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    ABSTRACT: Pain is common in people with dementia, representing a critical aspect of treatment and care. However, there remain considerable gaps in evidence to support pain assessment and treatment.
    British Medical Bulletin 09/2014; 111(1):139-48. · 4.36 Impact Factor
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    ABSTRACT: Background: The objective of this study was to examine the associations of agitation with the cerebrospinal fluid dementia biomarkers total-tau (T-tau), phosphorylated-tau (P-tau) and Aβ 1–42 . Methods: One hundred patients (mean age ± SD, 78.6 ± 7.5 years) with dementia and neuropsychiatric symptoms, of whom 67% were female, were included. Agitation was mea-sured using the Cohen-Mansfield Agitation Inventory (CMAI; 46.5 ± 11.8 points). Results: To-tal CMAI correlated with T-tau [r s (31) = 0.36, p = 0.04] and P-tau [r s (31) = 0.35, p = 0.05] in patients with Alzheimer's disease (AD; n = 33) but not in the total dementia population (n = 95). Conclusions: Our results suggest that tau-mediated pathology including neurofibrillary tangles and the intensity of the disease process might be associated with agitation in AD. This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only.
    Dementia and geriatric cognitive disorders extra. 08/2014; 4(2).
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    ABSTRACT: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are characterised by the presence of α-synuclein-containing Lewy bodies and Lewy neurites. However, both dementias also show variable degrees of Alzheimer's disease (AD) pathology (senile plaques and neurofibrillary tangles), particularly in areas of the cortex associated with higher cognitive functions. This study investigates the contribution of the individual and combined pathologies in determining the rate of cognitive decline. Cortical α-synuclein, phosphorylated-tau (phosphotau) and Aβ plaque pathology in 34 PDD and 55 DLB patients was assessed semi-quantitatively in four regions of the neocortex. The decline in cognition, assessed by Mini Mental State Examination, correlated positively with the cortical α-synuclein load. Patients also had varying degrees of senile Aβ plaque and phosphotau pathology. Regression analyses pointed to a combined pathology (Aβ plaque plus phosphotau plus α-synuclein positive features), particularly in the prefrontal cortex (BA9) and temporal lobe neocortex with the superior and middle temporal gyrus (BA 21, 22), being a major determining factor in the development of dementia. Thus, cognitive decline in Lewy body dementias is not a consequence of α-synuclein induced neurodegeneration alone but senile plaque and phosphorylated tau pathology also contribute to the overall deficits.
    Brain Pathology 08/2014; · 4.35 Impact Factor
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    ABSTRACT: To determine whether depressive symptoms are associated with medial temporal lobe atrophy in older people with and without Alzheimer disease (AD).
    Journal of Geriatric Psychiatry and Neurology 07/2014; · 3.53 Impact Factor
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    ABSTRACT: To investigate the effect on survival of treatment with memantine in patients with dementia with Lewy bodies (DLB) and Parkinson's disease with dementia (PDD).
    BMJ Open 07/2014; 4(7):e005158. · 2.06 Impact Factor
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    ABSTRACT: Aims: To examine the effects of galantamine and risperidone on agitation in patients with dementia. Methods: A total of 100 patients with dementia and neuropsychiatric symptoms (mean age ± SD: 78.6 ± 7.5 years; 67% female) were included in this 12-week, randomized, parallel-group, controlled, single-center trial. The participants received galantamine (n = 50; target dose: 24 mg) or risperidone (n = 50; target dose: 1.5 mg) for 12 weeks. Results: Both galantamine and risperidone treatment resulted in reduced agitation. However, risperidone showed a significant advantage over galantamine both at week 3 (mean difference in total Cohen-Mansfield Agitation Inventory score: 3.7 points; p = 0.03) and at week 12 (4.3 points; p = 0.01). Conclusions: Agitation improved in both groups, even if the treatment effects were more pronounced in the risperidone group; however, the effects on cognition and other aspects of tolerability were stronger with galantamine. © 2014 S. Karger AG, Basel.
    Dementia and Geriatric Cognitive Disorders 06/2014; 38(3-4):234-244. · 2.79 Impact Factor
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    ABSTRACT: The loss of zinc transporter 3 (ZnT3) has been implicated in age-related cognitive decline in mice, and the protein has been associated with plaques. We investigated the levels of ZnT3 and postsynaptic density protein 95 (PSD95), a marker of the postsynaptic terminal, in people with Parkinson's disease dementia (PDD, n = 31), dementia with Lewy bodies (DLB, n = 44), Alzheimer's disease (AD, n = 16), and controls (n = 24), using semiquantitative western blotting and immunohistochemistry in 3 cortical regions. Standardized cognitive assessments during life and semiquantitative scoring of amyloid β (Aβ), tau, and α-synuclein at postmortem were used to investigate the relationship between ZnT3 and PSD95, cognition and pathology. Associations were observed between ZnT3 and PSD95 levels in prefrontal cortex and cognitive impairment (p = 0.001 and p = 0.002, respectively) and between ZnT3 levels in the parietal cortex and cognitive impairment (p = 0.036). Associations were also seen between ZnT3 levels in cingulate cortex and severity of Aβ (p = 0.003) and tau (p = 0.011) pathologies. DLB and PDD were characterized by significant reductions of PSD95 (p < 0.05) and ZnT3 (p < 0.001) in prefrontal cortex compared with controls and AD. PSD95 levels in the parietal cortex were found to be decreased in AD cases compared with controls (p = 0.02) and PDD (p = 0.005). This study has identified Zn(2+) modulation as a possible novel target for the treatment of cognitive impairment in DLB and PDD and the potential for synaptic proteins to be used as a biomarker for the differentiation of DLB and PDD from AD.
    Neurobiology of Aging 06/2014; · 4.85 Impact Factor
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    ABSTRACT: DLB (Trønder-Brain) DLB (DemVest) AD (TrønderBrain) Healthy Controls (Trønder-Brain) Cases (Total) 156 103 53 519 643 Probable/Possible DLB 135/21 88/15 47/6 Objective To examine the role of APOE alleles in a Norwegian cohort of patients with dementia with Lewy bodies (DLB), compared to patients with Alzheimer's disease (AD) and healthy control individuals.
    The International Parkinson and Movement Disorder Society’s 18th International Congress of Parkinson's Disease and Movement Disorders, Stockholm; 06/2014
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    ABSTRACT: Background Pain is frequent and distressing in people with dementia, but no randomized controlled trials have evaluated the effect of analgesic treatment on pain intensity as a key outcome.Methods Three hundred fifty-two people with dementia and significant agitation from 60 nursing home units were included in this study. These units, representing 18 nursing homes in western Norway, were randomized to a stepwise protocol of treating pain (SPTP) or usual care. The SPTP group received acetaminophen, morphine, buprenorphine transdermal patch and pregabalin for 8 weeks, with a 4-week washout period. Medications were governed by the SPTP and each participant's existing prescriptions. We obtained pain intensity scores from 327 patients (intervention n = 164, control n = 163) at five time points assessed by the primary outcome measure, Mobilization-Observation-Behaviour-Intensity-Dementia-2 (MOBID-2) Pain Scale. The secondary outcome was activities of daily living (ADL). We used a linear intercept mixed model in a two-way repeated measures configuration to assess change over time and between groups.ResultsThe SPTP conferred significant benefit in MOBID-2 scores compared with the control group [average treatment effect (ATE) −1.388; p < 0.001] at week 8, and MOBID-2 scores worsened during the washout period (ATE = −0.701; p = 0.022). Examining different analgesic treatments, benefit was conferred to patients receiving acetaminophen compared with the controls at week 2 (ATE = −0.663; p = 0.010), continuing to increase until week 8 (ATE = −1.297; p < 0.001). Although there were no overall improvements in ADL, an increase was seen in the group receiving acetaminophen (ATE = +1.0; p = 0.022).Conclusion Pain medication significantly improved pain in the intervention group, with indications that acetaminophen also improved ADL function.
    European journal of pain (London, England) 06/2014; · 3.37 Impact Factor
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    ABSTRACT: Depression is a common symptom in dementia with Lewy bodies (DLB), Parkinson disease dementia (PDD), and Alzheimer disease (AD), yet its molecular basis remains unclear and current antidepressants do not appear to be effective. Cerebral zinc has been implicated in depression and synaptic dysfunction. We investigated the relationship between synaptic zinc regulation (for which zinc transporter 3 [ZnT3] is responsible) and depression in a large clinicopathologic study.
    The American journal of geriatric psychiatry: official journal of the American Association for Geriatric Psychiatry 05/2014; · 3.35 Impact Factor
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    ABSTRACT: Our aim was to assess cortical thickness in a large multicenter cohort of drug-naive patients with early Parkinson disease (PD), with and without mild cognitive impairment (MCI), and explore the cognitive correlates of regional cortical thinning. One hundred twenty-three newly diagnosed patients with PD and 56 healthy controls with 3-tesla structural MRI scans and complete neuropsychological assessment from the Parkinson's Progression Markers Initiative were included. Modified Movement Disorders Society Task Force level II criteria were applied to diagnose MCI in PD. FreeSurfer image processing and analysis software was used to measure cortical thickness across groups and the association with cognitive domains and tests. In patients with MCI, atrophy was found in temporal, parietal, frontal, and occipital areas compared with controls. Specific regional thinning in the right inferior temporal cortex was also found in cognitively normal patients. Memory, executive, and visuospatial performance was associated with temporoparietal and superior frontal thinning, suggesting a relationship between cognitive impairment and both anterior and posterior cortical atrophy in the whole patient sample. These findings confirm that MCI is associated with widespread cortical atrophy. In addition, they suggest that regional cortical thinning is already present at the time of diagnosis in patients with early, untreated PD who do not meet the criteria for MCI. Together, the results indicate that cortical thinning can serve as a marker for initial cognitive decline in early PD.
    Neurology 05/2014; · 8.30 Impact Factor

Publication Stats

13k Citations
1,766.91 Total Impact Points

Institutions

  • 2011–2014
    • Karolinska Institutet
      • KI-Alzheimercentrum - KI-ADRC
      Solna, Stockholm, Sweden
    • University of Louisville
      • Department of Neurology
      Louisville, KY, United States
    • Mayo Foundation for Medical Education and Research
      • Department of Neurology
      Scottsdale, AZ, United States
    • Akershus universitetssykehus
      Kristiania (historical), Oslo County, Norway
    • University of Naples Federico II
      Napoli, Campania, Italy
    • Instituto de Salud Carlos III
      Madrid, Madrid, Spain
  • 1996–2014
    • Stavanger University Hospital
      • • Department of Neurology
      • • Division of Psychiatry
      Stavenger, Rogaland, Norway
  • 2013
    • CSU Mentor
      Long Beach, California, United States
    • Biogen Idec
      Weston, Massachusetts, United States
    • Indiana University-Purdue University Indianapolis
      • Department of Neurology
      Indianapolis, Indiana, United States
  • 2007–2013
    • King's College London
      • Wolfson Centre for Age-Related Diseases
      London, ENG, United Kingdom
  • 2003–2013
    • University of Bergen
      • • Department of Public Health and Primary Health Care
      • • Institute of Medicine
      Bergen, Hordaland, Norway
  • 2012
    • Karolinska University Hospital
      • Center for Molecular Medicine (CMM)
      Stockholm, Stockholm, Sweden
  • 2011–2012
    • University of Oslo
      • Department of Neurology (NEUR)
      Kristiania (historical), Oslo County, Norway
  • 2010–2012
    • Lund University
      • Department of Clinical Sciences
      Lund, Skane, Sweden
    • Helse Fonna
      Haugesund, Rogaland, Norway
    • University at Buffalo, The State University of New York
      • Department of Neurology
      Buffalo, NY, United States
    • University of California, Los Angeles
      • Department of Neurology
      Los Angeles, California, United States
  • 2009
    • Haukeland University Hospital
      Bergen, Hordaland, Norway
  • 2008
    • University of Stavanger (UiS)
      Stavenger, Rogaland, Norway
  • 2006
    • The Newcastle upon Tyne Hospitals NHS Foundation Trust
      • Regional Neurosciences Centre
      Newcastle-on-Tyne, England, United Kingdom
    • Heinrich-Heine-Universität Düsseldorf
      • Neurologische Klinik
      Düsseldorf, North Rhine-Westphalia, Germany
  • 2004
    • Istanbul University
      • Department of Family Medicine (Istanbul Medical Faculty)
      İstanbul, Istanbul, Turkey
  • 1995–1996
    • NKS Olaviken, Hospital for Old Age Psychiatry
      Bergen, Hordaland, Norway