821 results found
Brooks D, Widespread microglial activation in multiple system atrophy, Movement Disorders, ISSN: 0885-3185
McGinnity CJ, Arstad E, Beck K, et al., 2019, Comment on "In Vivo [F-18]GE-179 Brain Signal Does Not Show NMDA-Specific Modulation with Drug Challenges in Rodents and Nonhuman Primates", ACS CHEMICAL NEUROSCIENCE, Vol: 10, Pages: 768-772, ISSN: 1948-7193
Lillethorup TP, Glud AN, Landeck N, et al., 2018, In vivo quantification of glial activation in minipigs overexpressing human alpha-synuclein, SYNAPSE, Vol: 72, ISSN: 0887-4476
Femminella G, Dani M, Wood M, et al., Microglial activation in early Alzheimer trajectory is associated with higher grey matter volume, Neurology, ISSN: 1526-632X
Objective: To investigate the influence of microglial activation in the early stages of Alzheimer’s disease trajectory, we assessed the relationship between microglial activation and grey matter volume and hippocampal volume in MCI patients.Methods: In this study, fifty-five participants (37 early stages MCI and 18 controls) underwent [11C]PBR28 PET, a marker of microglial activation; volumetric MRI to evaluate grey matter and hippocampal volumes as well as clinical and neuropsychometric evaluation. [11C]PBR28 VT(volume of distribution) was calculated using arterial input function and Logan Graphical analysis. Grey matter volume and hippocampal volumes were calculated from MRI for each subject. Statistical parametric mapping software was used to perform voxel-wise correlations and biological parametric mapping analysis. Amyloid status was assessed using [18F]Flutemetamol PET.Results: Higher [11C]PBR28 VT in different cortical areas correlated with higher grey matter volume in both amyloid positive and negative MCI. Additionally, higher hippocampal volume correlated with higher cortical [11C]PBR28 Logan VT.Conclusions: In this in vivo study, we have demonstrated that microglial activation quantified using [11C]PBR28 PET was associated with higher grey matter volume and higher hippocampal volume in MCI patients. This may suggest that microglial activation may not always be associatedwith neuronal damage, and indeed it may have beneficial effect in early stages of Alzheimer’s trajectory. While further longitudinal studies are necessary, these findings have significant implications on therapeutic strategies targeting microglial activation.
Sridharan S, Raffel J, Nandoskar A, et al., 2018, Confirmation of specific binding of the 18 kDa translocator protein (TSPO) radioligand [F-18]GE-180: a blocking study using XDB173 in multiple sclerosis, 34th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis (ECTRIMS), Publisher: SAGE PUBLICATIONS LTD, Pages: 421-422, ISSN: 1352-4585
Dani M, Wood M, Mizoguchi R, et al., 2018, Microglial activation correlates in vivo with both tau and amyloid in Alzheimer's disease, BRAIN, Vol: 141, Pages: 2740-2754, ISSN: 0006-8950
Parbo P, Ismail R, Sommerauer M, et al., 2018, Does inflammation precede tau aggregation in early Alzheimer's disease? A PET study, NEUROBIOLOGY OF DISEASE, Vol: 117, Pages: 211-216, ISSN: 0969-9961
Calsolaro V, Fan Z, Veronese M, et al., 2018, Novel third generation microglial marker flutriciclamide ([18F]GE180) in Alzheimer’s disease and mild cognitive impairment, Alzheimer's and Dementia, Vol: 14, Pages: P506-P506, ISSN: 1552-5260
Femminella G, Fan Z, Frangou E, et al., 2018, Peripheral insulin resistance does not correlate with cerebral glucose metabolic rate in non-diabetic Alzheimer’s patients, Alzheimer's and Dementia, Vol: 14, Pages: P1157-P1158, ISSN: 1552-5260
Minett T, Su L, Mak E, et al., 2018, Longitudinal diffusion tensor imaging changes in early Parkinson's disease: ICICLE-PD study, JOURNAL OF NEUROLOGY, Vol: 265, Pages: 1528-1539, ISSN: 0340-5354
Knudsen K, Fedorova TD, Hansen AK, et al., 2018, In-vivo staging of pathology in REM sleep behaviour disorder: a multimodality imaging case-control study, LANCET NEUROLOGY, Vol: 17, Pages: 618-628, ISSN: 1474-4422
Fan Z, Dani M, Femminella GD, et al., 2018, Parametric mapping using spectral analysis for C-11-PBR28 PET reveals neuroinflammation in mild cognitive impairment subjects, EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING, Vol: 45, Pages: 1432-1441, ISSN: 1619-7070
Stokholm MG, Iranzo A, Ostergaard K, et al., 2018, Extrastriatal monoaminergic dysfunction and enhanced microglial activation in idiopathic rapid eye movement sleep behaviour disorder, NEUROBIOLOGY OF DISEASE, Vol: 115, Pages: 9-16, ISSN: 0969-9961
Mattsson N, Groot C, Jansen WJ, et al., 2018, Prevalence of the apolipoprotein E epsilon 4 allele in amyloid beta positive subjects across the spectrum of Alzheimer's disease, ALZHEIMERS & DEMENTIA, Vol: 14, Pages: 913-924, ISSN: 1552-5260
McGinnity CJ, Barros DAR, Trigg W, et al., 2018, Simplifying [F-18]GE-179 PET: are both arterial blood sampling and 90-min acquisitions essential?, EJNMMI RESEARCH, Vol: 8, ISSN: 2191-219X
Sommerauer M, Hansen AK, Parbo P, et al., 2018, Decreased Noradrenaline Transporter Density in the Motor Cortex of Parkinson's Disease Patients, MOVEMENT DISORDERS, Vol: 33, Pages: 1006-1009, ISSN: 0885-3185
Hansen AK, Brooks DJ, Borghammer P, 2018, MAO-B Inhibitors Do Not Block In Vivo Flortaucipir([F-18]-AV-1451) Binding, MOLECULAR IMAGING AND BIOLOGY, Vol: 20, Pages: 356-360, ISSN: 1536-1632
Lillethorup TP, Glud AN, Alstrup AKO, et al., 2018, Nigrostriatal proteasome inhibition impairs dopamine neurotransmission and motor function in minipigs, EXPERIMENTAL NEUROLOGY, Vol: 303, Pages: 142-152, ISSN: 0014-4886
Jeppesen J, Otto M, Frederiksen Y, et al., 2018, Observations on muscle activity in REM sleep behavior disorder assessed with a semi-automated scoring algorithm, CLINICAL NEUROPHYSIOLOGY, Vol: 129, Pages: 541-547, ISSN: 1388-2457
Pasquini J, Ceravolo R, Qamhawi Z, et al., 2018, Progression of tremor in early stages of Parkinson's disease: a clinical and neuroimaging study, BRAIN, Vol: 141, Pages: 811-821, ISSN: 0006-8950
Sommerauer M, Fedorova TD, Hansen AK, et al., 2018, Evaluation of the noradrenergic system in Parkinson's disease: an C-11-MeNER PET and neuromelanin MRI study, BRAIN, Vol: 141, Pages: 496-504, ISSN: 0006-8950
Edison P, Brooks DJ, 2018, Role of Neuroinflammation in the Trajectory of Alzheimer's Disease and in vivo Quantification Using PET, JOURNAL OF ALZHEIMERS DISEASE, Vol: 64, Pages: S339-S351, ISSN: 1387-2877
Jansen WJ, Ossenkoppele R, Tijms BM, et al., 2018, Association of Cerebral Amyloid-beta Aggregation With Cognitive Functioning in Persons Without Dementia, JAMA PSYCHIATRY, Vol: 75, Pages: 84-95, ISSN: 2168-622X
Ismail R, Hansen AK, Parbo P, et al., 2018, The Effect of 40-Hz Light Therapy on Amyloid Load in Patients with Prodromal and Clinical Alzheimer's Disease., Int J Alzheimers Dis, Vol: 2018, ISSN: 2090-8024
Alzheimer's disease (AD) is a progressive neurodegenerative disorder. AD pathology is characterized by abnormal aggregation of the proteins amyloid-β (Aβ) and hyperphosphorylated tau. No effective disease modifying therapies are currently available. A short-duration intervention with 40 Hz light flicker has been shown to reduce brain Aβ load in transgenic mice. We aimed to test the effect of a similar short-duration 40 Hz light flicker regime in human AD patients. We utilized a Light Emitting Diode (LED) light bulb with a 40 Hz flicker. Six Aβ positive patients received 10 days of light therapy, had 2 hours of daily exposure, and underwent a postintervention PiB PET on day 11. After 10 days of light therapy, no significant decrease of PiB SUVR values was detected in any volumes of interest tested (primary visual cortex, visual association cortex, lateral parietal cortex, precuneus, and posterior cingulate) or in the total motor cortex, and longer treatments may be necessary to induce amyloid removal in humans.
Stokholm MG, Iranzo A, Ostergaard K, et al., 2017, Assessment of neuroinflammation in patients with idiopathic rapid-eye-movement sleep behaviour disorder: a case-control study, LANCET NEUROLOGY, Vol: 16, Pages: 789-796, ISSN: 1474-4422
Obeso JA, Stamelou M, Goetz CG, et al., 2017, Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy., Mov Disord, Vol: 32, Pages: 1264-1310
This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society.
Lawson RA, Yarnall AJ, Duncan GW, et al., 2017, Stability of mild cognitive impairment in newly diagnosed Parkinson's disease., J Neurol Neurosurg Psychiatry, Vol: 88, Pages: 648-652
BACKGROUND: Mild cognitive impairment (MCI) is common in early Parkinson's disease (PD). We evaluated the stability of PD-MCI over time to determine its clinical utility as a marker of disease. METHODS: 212 newly diagnosed participants with PD were recruited into a longitudinal study and reassessed after 18 and 36 months. Participants completed a range of clinical and neuropsychological assessments. PD-MCI was classified using Movement Disorders Society Task Force level I (Montreal Cognitive Assessment <26) and level II (using cut-offs of 1, 1.5 and 2SD) criteria. RESULTS: After 36 months, 75% of participants returned; 8% of patients had developed a dementia all of which were previously PD-MCI. Applying level I criteria, 70% were cognitively stable, 19% cognitively declined and 11% improved over 36 months. Applying level II criteria (1, 1.5 and 2SD), 25% were cognitively stable, 41% cognitively declined, 15% improved and 19% fluctuated over 36 months. 18% of participants reverted to normal cognition from PD-MCI. DISCUSSION: Cognitive impairment in PD is complex, with some individuals' function fluctuating over time and some reverting to normal cognition. PD-MCI level I criteria may have greater clinical convenience, but more comprehensive level II criteria with 2SD cut-offs may offer greater diagnostic certainty.
Dani M, Wood M, Mizoguchi R, et al., 2017, Different modelling approaches for tau tracer 18F-AV1451 in mild cognitive impairment and Alzheimer's disease, Alzheimer's and Dementia, Vol: 13, Pages: P291-P292, ISSN: 1552-5260
Femminella G, Dani M, Wood M, et al., 2017, Microglial activation is associated with higher grey matter density and hippocampal volume in MCi subjects, Alzheimer's and Dementia, Vol: 13, Pages: P921-P921, ISSN: 1552-5260
Fan Z, Femminella GD, Calsolaro V, et al., 2017, Strategies to develop parametric maps for TSPO PET tracer [11C]-PBR28 in patients with mild cognitive impairment, Alzheimer's and Dementia, Vol: 13, Pages: P288-P289, ISSN: 1552-5260
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