ProfessorDavidBrooks

Taylor S, Gafton J, Shah B, Pagano G, Chaudhuri KR, Brooks DJ, Pavese Net al., 2016, Progression of nonmotor symptoms in subgroups of patients with non-dopamine-deficient Parkinsonism, MOVEMENT DISORDERS, Vol: 31, Pages: 344-351, ISSN: 0885-3185

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• Citations: 21

Brooks DJ, Tambasco N, 2016, Imaging synucleinopathies., Movement Disorders, Vol: 31, Pages: 814-829, ISSN: 1531-8257

In this review the structural and functional imaging changes associated with the synucleinopathies PD, MSA, and dementias associated with Lewy bodies are reviewed. The role of imaging for supporting differential diagnosis, detecting subclinical disease, and following disease progression is discussed and its potential use for monitoring disease progression is debated. © 2016 International Parkinson and Movement Disorder Society.

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Lingford-Hughes A, Myers J, Watson B, Reid AG, Kalk N, Feeney A, Hammers A, Riaño-Barros DA, McGinnity CJ, Taylor LG, Rosso L, Brooks DJ, Turkheimer F, Nutt DJet al., 2016, Using [11C]Ro15 4513 PET to characterise GABA-benzodiazepine receptors in opiate addiction: Similarities and differences with alcoholism, Neuroimage, Vol: 132, Pages: 1-7, ISSN: 1095-9572

The importance of the GABA-benzodiazepine receptor complex and its subtypes are increasingly recognised inaddiction. Using the α1/α5 benzodiazepine receptor PET radioligand [ 23 11C]Ro15 4513, we previously showed reducedbinding in the nucleus accumbens and hippocampus in abstinent alcohol dependence. We proposed that 24reduced [ 25 11C]Ro15 4513 binding in the nucleus accumbens was a marker of addiction whilst the reduction in hippocampusand positive relationship with memory was a consequence of chronic alcohol abuse. To examine this 26further we assessed [ 27 11C]Ro15 4513 binding in another addiction, opiate dependence, and used spectral analysisto estimate contributions of α1 and α5 subtypes to [ 28 11C]Ro15 4513 binding in opiate and previously acquired alcohol-dependentgroups. Opiate substitute maintained opiate-dependent men (n = 12) underwent an [ 29 11C]Ro154513 PET scan and compared with matched healthy controls (n = 13). We found a significant reduction in 30[ 31 11C]Ro15 4513 binding in the nucleus accumbens in the opiate-dependent compared with the healthy controlgroup. There was no relationship between [ 32 11C]Ro15 4513 binding in the hippocampus with memory. Wefound that reduced [ 33 11C]Ro15 4513 binding was associated with reduced α5 but not α1 subtypes in the opiate-dependentgroup. This was also seen in an alcohol-dependent group where an association between memory 34performance and [ 35 11C]Ro15 4513 binding was primarily driven by α5 and not α1 subtype. We suggest that reducedα5 levels in the nucleus accumbens are associated with addiction since we have now shown this in depen- 36dence to two pharmacologically different substances, alcohol and opiates.

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Pagano G, Ferrara N, Brooks DJ, Pavese Net al., 2016, Age at onset and Parkinson disease phenotype, Neurology, Vol: 86, Pages: 1400-1407, ISSN: 0028-3878

Objective: To explore clinical phenotype and characteristics of Parkinson disease (PD) at different ages at onset in recently diagnosed patients with untreated PD.Methods: We have analyzed baseline data from the Parkinson's Progression Markers Initiative database. Four hundred twenty-two patients with a diagnosis of PD confirmed by DaTSCAN imaging were divided into 4 groups according to age at onset (onset younger than 50 years, 50–59 years, 60–69 years, and 70 years or older) and investigated for differences in side, type and localization of symptoms, occurrence/severity of motor and nonmotor features, nigrostriatal function, and CSF biomarkers.Results: Older age at onset was associated with a more severe motor and nonmotor phenotype, a greater dopaminergic dysfunction on DaTSCAN, and reduction of CSF α-synuclein and total tau. The most common presentation was the combination of 2 or 3 motor symptoms (bradykinesia, resting tremor, and rigidity) with rigidity being more common in the young-onset group. In about 80% of the patients with localized onset, the arm was the most affected part of the body, with no difference across subgroups.Conclusions: Although the presentation of PD symptoms is similar across age subgroups, the severity of motor and nonmotor features, the impairment of striatal binding, and the levels of CSF biomarkers increase with age at onset. The variability of imaging and nonimaging biomarkers in patients with PD at different ages could hamper the results of future clinical trials.

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Crocce M, Carretero J, Bauer AH, Ross AJ, Sevilla-Noarbe I, Giannantonio T, Sobreira F, Sanchez J, Gaztanaga E, Kind MC, Sanchez C, Bonnett C, Benoit-Levy A, Brunner RJ, Carnero Rosell A, Cawthon R, Fosalba P, Hartley W, Kim EJ, Leistedt B, Miquel R, Peiris HV, Percival WJ, Rosenfeld R, Rykoff ES, Sanchez E, Abbott T, Abdalla FB, Allam S, Banerji M, Bernstein GM, Bertin E, Brooks D, Buckley-Geer E, Burke DL, Capozzi D, Castander FJ, Cunha CE, D'Andrea CB, Da Costa LN, Desai S, Diehl HT, Eifler TF, Evrard AE, Fausti Neto A, Fernandez E, Finley DA, Flaugher B, Frieman J, Gerdes DW, Gruen D, Gruendl RA, Gutierrez G, Honscheid K, James DJ, Kuehn K, Kuropatkin N, Lahav O, Li TS, Lima M, Maia MAG, March M, Marshall JL, Martini P, Melchior P, Miller CJ, Neilsen E, Nichol RC, Nord B, Ogando R, Plazas AA, Romer AK, Sako M, Santiago B, Schubnell M, Smith RC, Soares-Santos M, Suchyta E, Swanson MEC, Tarle G, Thaler J, Thomas D, Vikram V, Walker AR, Wechsler RH, Weller J, Zuntz Jet al., 2016, Galaxy clustering, photometric redshifts and diagnosis of systematics in the DES Science Verification data, MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY, Vol: 455, Pages: 4301-4324, ISSN: 0035-8711

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• Citations: 71

Pavese N, Brooks DJ, 2016, Atypical Parkinsonian Syndromes, IMAGING OF NEURODEGENERATIVE DISORDERS, Publisher: GEORG THIEME VERLAG, Pages: 180-185, ISBN: 978-1-60406-854-2

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Ray Chaudhuri K, Rojo JM, Schapira AHV, Brooks DJ, Stocchi F, Odin P, Antonini A, Brown RG, Martinez-Martin Pet al., 2016, Correction: A Proposal for a Comprehensive Grading of Parkinson's Disease Severity Combining Motor and Non-Motor Assessments: Meeting an Unmet Need., PLoS One, Vol: 11

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Scott G, Hellyer PJ, Ramlackhansingh AF, Brooks DJ, Matthews PM, Sharp DJet al., 2015, Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage, Journal of Neuroinflammation, Vol: 12, ISSN: 1742-2094

BackgroundTraumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo.FindingsUsing [11C]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury. Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage.ConclusionsThese findings support a link between axonal damage and persistent inflammation after brain injury.

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Mak E, Su L, Williams G, Lawson R, Yarnall A, Gordon D, Adrian O, Tien K, Brooks D, Rowe J, Barker R, Burn D, O'Brien Jet al., 2015, Baseline and longitudinal grey matter changes in newly diagnosed Parkinson's disease: ICICLE-PD study, Publisher: CAMBRIDGE UNIV PRESS, Pages: S159-S160, ISSN: 1041-6102

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Dani M, Brooks DJ, Edison P, 2015, Tau imaging in neurodegenerative diseases, European Journal of Nuclear Medicine and Molecular Imaging, Vol: 43, Pages: 1139-1150, ISSN: 1619-7089

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Fan Z, Okello AA, Brooks DJ, Edison Pet al., 2015, Longitudinal influence of microglial activation and amyloid on neuronal function in Alzheimer’s disease, Brain, Vol: 138, Pages: 3685-3698, ISSN: 1460-2156

Amyloid deposition, tangle formation, neuroinflammation and neuronal dysfunction are pathological processes involved in Alzheimer’s disease. However, the relative role of these processes in driving disease progression is still unclear. The aim of this positron emission tomography study was to: (i) investigate longitudinal changes of microglial activation, amyloid and glucose metabolism; and (ii) assess the temporospatial relationship between these three processes in Alzheimer’s disease. A group of eight patients with a diagnosis of Alzheimer’s disease (66 ± 4.8 years) and 14 healthy controls (65 ± 5.5 years) underwent T1 and T2 magnetic resonance imaging, along with 11C-(R)-PK11195, 11C-Pittsburgh compound B and 18F-fluorodeoxyglucose positron emission tomography scans for microglial activation, amyloid deposition and glucose metabolism. All patients were followed-up with repeated magnetic resonance imaging and three positron emission tomography scans after 16 months. Parametric maps were interrogated using region of interest analysis, Statistical Parametric Mapping, and between-group correlation analysis at voxel-level using Biological Parametric Mapping. At baseline, patients with Alzheimer’s disease showed significantly increased microglial activation compared to the control subjects. During follow-up, for the first time, we found that while there is a progressive reduction of glucose metabolism, there was a longitudinal increase of microglial activation in the majority of the patients with Alzheimer’s disease. Voxel-wise correlation analysis revealed that microglial activation in patients with Alzheimer’s disease was positively correlated with amyloid deposition and inversely correlated with regional cerebral metabolic rate at voxel level over time. Even though one of the limitations of this study is the lack of longitudinal follow-up of healthy control subjects, this study demonstrates that there is persistent n

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Mak E, Su L, Williams GB, Firbank MJ, Lawson RA, Yarnall AJ, Duncan GW, Owen AM, Khoo TK, Brooks DJ, Rowe JB, Barker RA, Burn DJ, O'Brien JTet al., 2015, Baseline and longitudinal grey matter changes in newly diagnosed Parkinson's disease: ICICLE-PD study, BRAIN, Vol: 138, Pages: 2974-2986, ISSN: 0006-8950

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• Citations: 158

Qamhawi Z, Towey D, Shah B, Pagano G, Seibyl J, Marek K, Borghammer P, Brooks DJ, Pavese Net al., 2015, Clinical correlates of raphe serotonergic dysfunction in early Parkinson's disease, BRAIN, Vol: 138, Pages: 2964-2973, ISSN: 0006-8950

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• Citations: 136

McGinnity CJ, Koepp MJ, Hammers A, Barros DAR, Pressler RM, Luthra S, Jones PA, Trigg W, Micallef C, Symms MR, Brooks DJ, Duncan JSet al., 2015, NMDA receptor binding in focal epilepsies, JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, Vol: 86, Pages: 1150-1157, ISSN: 0022-3050

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• Citations: 36

Simuni T, Caspell-Garcia C, Coffey C, Chahine LM, Lasch S, Oertel WH, Mayer G, Hoegl B, Postuma R, Videnovic A, Amara AW, Marek Ket al., 2015, Correlates of Excessive Daytime Sleepiness in De Novo Parkinson's Disease: A Case Control Study, MOVEMENT DISORDERS, Vol: 30, Pages: 1371-1381, ISSN: 0885-3185

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• Citations: 60

Varley J, Brooks DJ, Edison P, 2015, Imaging neuroinflammation in Alzheimer's disease and other dementias: Recent advances and future directions, ALZHEIMERS & DEMENTIA, Vol: 11, Pages: 1110-1120, ISSN: 1552-5260

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• Citations: 59

Dani M, Edison P, Brooks DJ, 2015, Imaging biomarkers in tauopathies, Parkinsonism & Related Disorders, Vol: 22, Pages: S26-S28, ISSN: 1353-8020

Abnormally aggregated tau protein is central to the pathophysiology of Alzheimer's disease, frontotemporal dementia variants, progressive supranuclear palsy, corticobasal degeneration and chronic traumatic encephalopathy. The post-mortem cortical density of hyperphosphorylated tau tangles correlates with pre-morbid cognitive dysfunction and neuron loss. Selective PET ligands including [18F]THK5117, [18F]THK5351, [18F]AV1451 (T807) and [11C]PBB3 now provide in vivo imaging information about the timing and distribution of tau in the early phases of neurodegenerative diseases. They are potential imaging biomarkers for both supporting diagnosis and tracking disease progression. Here, we discuss the challenges posed in developing selective tau ligands as biomarkers, their state of development and the new clinical information that has been revealed.

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Senda M, Brooks DJ, Farrar G, Somer EJ, Paterson CL, Sasaki M, McParland BJet al., 2015, The clinical safety, biodistribution and internal radiation dosimetry of flutemetamol (<SUP>18</SUP>F) injection in healthy Japanese adult volunteers, ANNALS OF NUCLEAR MEDICINE, Vol: 29, Pages: 627-635, ISSN: 0914-7187

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• Citations: 7

Vikram V, Chang C, Jain B, Bacon D, Amara A, Becker MR, Bernstein G, Bonnett C, Bridle S, Brout D, Busha M, Frieman J, Gaztanaga E, Hartley W, Jarvis M, Kacprzak T, Kovacs A, Lahav O, Leistedt B, Lin H, Melchior P, Peiris H, Rozo E, Rykoff E, Sanchez C, Sheldon E, Troxel MA, Wechsler R, Zuntz J, Abbott T, Abdalla FB, Armstrong R, Banerji M, Bauer AH, Benoit-Levy A, Bertin E, Brooks D, Buckley-Geer E, Burke DL, Capozzi D, Carnero Rosell A, Kind MC, Castander FJ, Crocce M, Cunha CE, D'Andrea CB, da Costa LN, Depoy DL, Desai S, Diehl HT, Dietrich JP, Estrada J, Evrard AE, Fausti Neto A, Fernandez E, Flaugher B, Fosalba P, Gerdes D, Gruen D, Gruendl RA, Honscheid K, James D, Kent S, Kuehn K, Kuropatkin N, Li TS, Maia MAG, Makler M, March M, Marshall J, Martini P, Merritt KW, Miller CJ, Miquel R, Neilsen E, Nichol RC, Nord B, Ogando R, Plazas AA, Romer AK, Roodman A, Sanchez E, Scarpine V, Sevilla I, Smith RC, Soares-Santos M, Sobreira F, Suchyta E, Swanson MEC, Tarle G, Thaler J, Thomas D, Walker AR, Weller Jet al., 2015, Wide-field lensing mass maps from Dark Energy Survey science verification data: Methodology and detailed analysis, PHYSICAL REVIEW D, Vol: 92, ISSN: 1550-7998

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• Citations: 47

Duncan GW, Firbank MJ, Yarnall AJ, Khoo TK, Brooks DJ, Barker RA, Burn DJ, O'Brien JTet al., 2015, Gray and white matter imaging: a biomarker for cognitive impairment in early Parkinson's disease?, Movement Disorders, Vol: 31, Pages: 103-110, ISSN: 1531-8257

BackgroundThe aim of this work was to investigate the cortical and white matter changes that underlie cognitive impairment in patients with incident Parkinson's disease (PD) disease using voxel-based morphometry and diffusion tensor imaging.MethodsNewly diagnosed nondemented PD (n = 125) and control subjects (n = 50) were recruited from the Incidence of Cognitive Impairment in Cohorts with Longitudinal Evaluation in Parkinson's Disease Study and completed cognitive assessments and 3T structural and diffusion tensor MR imaging. Voxel-based morphometry was performed to investigate the relationship between gray matter volume and cognitive ability. Microstructural white matter changes were assessed with diffusion tensor imaging measures of fractional anisotropy and mean diffusivity using tract-based spatial statistics.ResultsIncreased mean diffusivity was observed bilaterally in subjects with PD, relative to controls (P = 0.019). Increased mean diffusivity was associated with performance on the semantic fluency and Tower of London tasks in frontal and parietal white matter tracts, including the cingulum, superior longitudinal fasciculus, inferior longitudinal fasciculus, and inferior fronto-occipital fasciculus. There was no difference in total gray matter volume between groups; however, bilateral reductions in frontal and parietal gray matter volume were associated with reduced performance on measures of executive function in PD subjects.ConclusionsAt the earliest stages of PD, regionally specific increases in central white matter mean diffusivity are present and suggest early axonal damage. Such changes are not accompanied by significant gray matter volume loss and are consistent with proposed models of pathological progression of the disease. Structural MRI, especially diffusion tensor imaging analysis, offers potential as a noninvasive biomarker reflecting cognitive impairment in PD.

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Fan Z, Aman Y, Ahmed I, Chetelat G, Landeau B, Chaudhuri KR, Brooks DJ, Edison Pet al., 2015, Influence of microglial activation on neuronal function in Alzheimer's and Parkinson's disease dementia, Alzheimers & Dementia, Vol: 11, Pages: 608-621, ISSN: 1552-5260

BackgroundAlzheimer's disease (AD) and Parkinson's disease (PD) are the two common neurodegenerative diseases characterized by progressive neuronal dysfunction in the presence of pathological microglial activation.Methods10 AD, 10 mild cognitive impairment (MCI), 11 PD dementia (PDD), and 16 controls underwent magnetic resonance imaging, [11C](R)PK11195 (1‐[2‐chlorophenyl]‐N‐methyl‐N‐[1‐methyl‐propyl]‐3‐isoquinoline carboxamide), [11C]PIB (11C‐Pittsburgh compound B), [18F]FDG‐PET (18F‐2‐fluoro‐2‐deoxyglucose positron emission tomography) scans. Parametric images were interrogated using region of interest (ROI), biological parametric mapping (BPM) and statistical parametric mapping analysis, and neuropsychometric tests.ResultsUsing BPM analysis, AD, MCI, and PDD subjects demonstrated significant correlation between increased microglial activation and reduced glucose metabolism (rCMRGlc). AD and MCI subjects also showed significant positive correlation between amyloid and microglial activation. Levels of cortical microglial activation were negatively correlated with Mini‐Mental State Examination in both AD and PDD.ConclusionThe significant inverse correlations between cortical levels of microglial activation and rCMRGlc in AD and PDD suggest cortical neuroinflammation may drive neuronal dysfunction in these dementias.

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Senda M, Yamamoto Y, Sasaki M, Yamane T, Brooks DJ, Farrar G, McParland B, Heurling Ket al., 2015, An exploratory efficacy study of the amyloid imaging agent [<SUP>18</SUP>F]flutemetamol in Japanese Subjects, ANNALS OF NUCLEAR MEDICINE, Vol: 29, Pages: 391-399, ISSN: 0914-7187

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• Citations: 2

Jansen WJ, Ossenkoppele R, Knol DL, Tijms BM, Scheltens P, Verhey FRJ, Visser PJ, Amyloid Biomarker Study Group, Aalten P, Aarsland D, Alcolea D, Alexander M, Almdahl IS, Arnold SE, Baldeiras I, Barthel H, van Berckel BNM, Bibeau K, Blennow K, Brooks DJ, van Buchem MA, Camus V, Cavedo E, Chen K, Chetelat G, Cohen AD, Drzezga A, Engelborghs S, Fagan AM, Fladby T, Fleisher AS, van der Flier WM, Ford L, Förster S, Fortea J, Foskett N, Frederiksen KS, Freund-Levi Y, Frisoni GB, Froelich L, Gabryelewicz T, Gill KD, Gkatzima O, Gómez-Tortosa E, Gordon MF, Grimmer T, Hampel H, Hausner L, Hellwig S, Herukka S-K, Hildebrandt H, Ishihara L, Ivanoiu A, Jagust WJ, Johannsen P, Kandimalla R, Kapaki E, Klimkowicz-Mrowiec A, Klunk WE, Köhler S, Koglin N, Kornhuber J, Kramberger MG, Van Laere K, Landau SM, Lee DY, de Leon M, Lisetti V, Lleó A, Madsen K, Maier W, Marcusson J, Mattsson N, de Mendonça A, Meulenbroek O, Meyer PT, Mintun MA, Mok V, Molinuevo JL, Møllergård HM, Morris JC, Mroczko B, Van der Mussele S, Na DL, Newberg A, Nordberg A, Nordlund A, Novak GP, Paraskevas GP, Parnetti L, Perera G, Peters O, Popp J, Prabhakar S, Rabinovici GD, Ramakers IHGB, Rami L, Resende de Oliveira C, Rinne JO, Rodrigue KM, Rodríguez-Rodríguez E, Roe CM, Rot U, Rowe CC, Rüther E, Sabri O, Sanchez-Juan P, Santana I, Sarazin M, Schröder J, Schütte C, Seo SW, Soetewey F, Soininen H, Spiru L, Struyfs H, Teunissen CE, Tsolaki M, Vandenberghe R, Verbeek MM, Villemagne VL, Vos SJB, van Waalwijk van Doorn LJC, Waldemar G, Wallin A, Wallin ÅK, Wiltfang J, Wolk DA, Zboch M, Zetterberg Het al., 2015, Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis., JAMA, Vol: 313, Pages: 1924-1938

IMPORTANCE: Cerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies. OBJECTIVE: To use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI). DATA SOURCES: Relevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE and Web of Science databases and through personal communication with investigators. STUDY SELECTION: Studies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity. DATA EXTRACTION AND SYNTHESIS: Individual records were provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies. MAIN OUTCOMES AND MEASURES: Prevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations. RESULTS: The prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95% CI, 8%-13%) to 44% (95% CI, 37%-51%) among participants with normal cognition; from 12% (95% CI, 8%-18%) to 43% (95% CI, 32%-55%) among patients with SCI; and from 27% (95% CI, 23%-32%) to 71% (95% CI, 66%-76%) among patients with MCI. APOE-ε4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE ε4ε4 carriers, 50 years for ε2ε4 carriers, 55 years for &epsil

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Ossenkoppele R, Jansen WJ, Rabinovici GD, Knol DL, van der Flier WM, van Berckel BNM, Scheltens P, Visser PJet al., 2015, Prevalence of Amyloid PET Positivity in Dementia Syndromes A Meta-analysis, JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, Vol: 313, Pages: 1939-1949, ISSN: 0098-7484

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• Citations: 411

Fan Z, Harold D, Pasqualetti G, Williams J, Brooks DJ, Edison Pet al., 2015, Can Studies of Neuroinflammation in a TSPO Genetic Subgroup (HAB or MAB) Be Applied to the Entire AD Cohort?, JOURNAL OF NUCLEAR MEDICINE, Vol: 56, Pages: 707-713, ISSN: 0161-5505

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• Citations: 26

Pasqualetti G, Brooks DJ, Edison P, 2015, The Role of Neuroinflammation in Dementias, CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS, Vol: 15, ISSN: 1528-4042

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• Citations: 94

Brooks DJ, 2015, Neuroimaging in Parkinson's disease: a future perspective, NEURODEGENERATIVE DISEASE MANAGEMENT, Vol: 5, Pages: 105-108, ISSN: 1758-2024

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• Citations: 1

Smith R, Wu K, Hart T, Loane C, Brooks DJ, Bjorklund A, Odin P, Piccini P, Politis Met al., 2015, The role of pallidal serotonergic function in Parkinson's disease dyskinesias: a positron emission tomography study, NEUROBIOLOGY OF AGING, Vol: 36, Pages: 1736-1742, ISSN: 0197-4580

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• Citations: 35

Heneka MT, Carson MJ, El Khoury J, Landreth GE, Brosseron F, Feinstein DL, Jacobs AH, Wyss-Coray T, Vitorica J, Ransohoff RM, Herrup K, Frautschy SA, Finsen B, Brown GC, Verkhratsky A, Yamanaka K, Koistinaho J, Latz E, Halle A, Petzold GC, Town T, Morgan D, Shinohara ML, Perry VH, Holmes C, Bazan NG, Brooks DJ, Hunot S, Joseph B, Deigendesch N, Garaschuk O, Boddeke E, Dinarello CA, Breitner JC, Cole GM, Golenbock DT, Kummer MPet al., 2015, Neuroinflammation in Alzheimer's disease, LANCET NEUROLOGY, Vol: 14, Pages: 388-405, ISSN: 1474-4422

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• Citations: 3401

Chang C, Busha MT, Wechsler RH, Refregier A, Amara A, Rykoff E, Becker MR, Bruderer C, Gamper L, Leistedt B, Peiris H, Abbott T, Abdalla FB, Balbinot E, Banerji M, Bernstein RA, Bertin E, Brooks D, Carner A, Desai S, da Costa LN, Cunha CE, Eifler T, Evrard AE, Rausti Neto A, Gerdes D, Gruen D, James D, Kuehn K, Maia MAG, Makler M, Ogando R, Plazas A, Sanchez E, Santiago B, Schubnell M, Sevilla-Noarbe I, Smith C, Soares-Santos M, Suchyta E, Swanson MEC, Tarle G, Zuntz Jet al., 2015, MODELING THE TRANSFER FUNCTION FOR THE DARK ENERGY SURVEY, ASTROPHYSICAL JOURNAL, Vol: 801, ISSN: 0004-637X

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• Citations: 30