Imperial College London

ProfessorDavidBrooks

Faculty of MedicineDepartment of Medicine

Visiting Professor
 
 
 
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Contact

 

david.brooks

 
 
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Assistant

 

Ms Hyacinth Henry +44 (0)20 3313 3172

 
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Location

 

U106Block B Hammersmith HospitalHammersmith Campus

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Summary

 

Publications

Publication Type
Year
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827 results found

Femminella GD, Frangou E, Love SB, Busza G, Holmes C, Ritchie C, Lawrence R, McFarlane B, Tadros G, Ridha BH, Bannister C, Walker Z, Archer H, Coulthard E, Underwood BR, Prasanna A, Koranteng P, Karim S, Junaid K, McGuinness B, Nilforooshan R, Macharouthu A, Donaldson A, Thacker S, Russell G, Malik N, Mate V, Knight L, Kshemendran S, Harrison J, Brooks DJ, Passmore AP, Ballard C, Edison Pet al., 2019, Evaluating the effects of the novel GLP-1 analogue liraglutide in Alzheimer's disease: study protocol for a randomised controlled trial (ELAD study)., Trials, Vol: 20

BACKGROUND: Liraglutide is a glucagon-like peptide-1 (GLP-1) analogue currently approved for type 2 diabetes and obesity. Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity and cerebral glucose uptake, and increasing the proliferation of neuronal progenitor cells. The primary objective of the study is to evaluate the change in cerebral glucose metabolic rate after 12 months of treatment with liraglutide in participants with Alzheimer's disease compared to those who are receiving placebo. METHODS/DESIGN: ELAD is a 12-month, multi-centre, randomised, double-blind, placebo-controlled, phase IIb trial of liraglutide in participants with mild Alzheimer's dementia. A total of 206 participants will be randomised to receive either liraglutide or placebo as a daily injection for a year. The primary outcome will be the change in cerebral glucose metabolic rate in the cortical regions (hippocampus, medial temporal lobe, and posterior cingulate) from baseline to follow-up in the treatment group compared with the placebo group. The key secondary outcomes are the change from baseline to 12 months in z scores for clinical and cognitive measures (Alzheimer's Disease Assessment Scale-Cognitive Subscale and Executive domain scores of the Neuropsychological Test Battery, Clinical Dementia Rating Sum of Boxes, and Alzheimer's Disease Cooperative Study-Activities of Daily Living) and the incidence and severity of treatment-emergent adverse events or clinically important changes in safety assessments. Other secondary outcomes are 12-month change in magnetic resonance imaging volume, diffusion tensor imaging parameters, reduction in microglial activation in a subgroup of participants, reduction in tau formation and change in amyloid levels in a subgroup of participants measured by tau and amyloid imaging, and changes in composite scores u

JOURNAL ARTICLE

Femminella GD, Dani M, Wood M, Fan Z, Calsolaro V, Atkinson R, Edginton T, Hinz R, Brooks DJ, Edison Pet al., 2019, Microglial activation in early Alzheimer trajectory is associated with higher gray matter volume., Neurology, Vol: 92, Pages: e1331-e1343

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 gray matter volume and hippocampal volume in patients with mild cognitive impairment (MCI). METHODS: In this study, 55 participants (37 with early stages of MCI and 18 controls) underwent [11C]PBR28 PET, a marker of microglial activation; volumetric MRI to evaluate gray 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. Gray matter volume and hippocampal volumes were calculated from MRI for each participant. 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 gray matter volume in both amyloid-positive and -negative MCI. In addition, 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 gray matter volume and higher hippocampal volume in patients with MCI. This might suggest that microglial activation may not always be associated with neuronal damage, and indeed it may have a beneficial effect in the early stages of the Alzheimer trajectory. While further longitudinal studies are necessary, these findings have significant implications on therapeutic strategies targeting microglial activation.

JOURNAL ARTICLE

Schubert JJ, Veronese M, Marchitelli L, Bodini B, Tonietto M, Stankoff B, Brooks DJ, Bertoldo A, Edison P, Turkheimer Fet al., 2019, Dynamic 11C-PiB PET shows cerebrospinal fluid flow alterations in Alzheimer's disease and multiple sclerosis., J Nucl Med

Cerebrospinal fluid (CSF) plays an important role in the clearance of solutes and maintenance of brain homeostasis. 11C-PiB PET was recently proposed as a tool for detection of CSF clearance alterations in Alzheimer's disease. The current study seeks to investigate the magnitude of 11C-PiB PET signal in the lateral ventricles of an independent group of Alzheimer's and mild cognitive impairment subjects. We have also evaluated multiple sclerosis as a model of disease with CSF clearance alterations without amyloid-beta tissue accumulation. Methods: A set of Alzheimer's and mild cognitive impairment subjects and a set of multiple sclerosis subjects with matched healthy controls underwent MRI and dynamic 11C-PiB PET. Manual lateral ventricle regions of interest were generated from MRI data. PET data was analysed using a simplified reference tissue model with cerebellum or a supervised reference region, for the Alzheimer's and multiple sclerosis datasets, respectively. Magnitude of 11C-PiB signal in the lateral ventricles was calculated as area under curve from 35 to 80 minutes and standard uptake value ratio (SUVR) from 50 to 70 minutes. Compartmental modelling analysis was performed on a separate dataset containing Alzheimer's and matched healthy control data with an arterial input function to further understand the kinetics of the lateral ventricular 11C-PiB signal. Results: Analysis of variance revealed significant group differences in lateral ventricular SUVR across the Alzheimer's, mild cognitive impairment, and healthy control groups (P = 0.004). Additional pairwise comparisons revealed significantly lower lateral ventricular SUVR in Alzheimer's compared to healthy controls (p<0.001) and mild cognitive impairment (P = 0.029). Lateral ventricular SUVR was also significantly lower in multiple sclerosis compared to healthy controls (P = 0.008). Compartmental modelling analysis revealed significantly lower uptake rates of 11C-PiB signal from blood (P = 0.005) and b

JOURNAL ARTICLE

Dafsari HS, Martinez-Martin P, Rizos A, Trost M, dos Santos Ghilardi MG, Reddy P, Sauerbier A, Petry-Schmelzer JN, Kramberger M, Borgemeester RWK, Barbe MT, Ashkan K, Silverdale M, Evans J, Odin P, Fonoff ET, Fink GR, Henriksen T, Ebersbach G, Pirtosek Z, Visser-Vandewalle V, Antonini A, Timmermann L, Chaudhuri KR, Schrag A, Weintraub D, Barone P, Brooks DJ, Brown RG, Jenner P, Jeon B, Lyons K, Pavese N, Politis M, Postuma RB, Schapira A, Stocchi F, Tsuboi Yet al., 2019, EuroInf 2: Subthalamic stimulation, apomorphine, and levodopa infusion in Parkinson's disease, MOVEMENT DISORDERS, Vol: 34, Pages: 353-365, ISSN: 0885-3185

JOURNAL ARTICLE

Moller A, Thomsen KR, Brooks DJ, Mouridsen K, Blicher JU, Hansen K, Lou HCet al., 2019, Attenuation of dopamine-induced GABA release in problem gamblers, BRAIN AND BEHAVIOR, Vol: 9, ISSN: 2162-3279

JOURNAL ARTICLE

Sridharan S, Raffel J, Nandoskar A, Record C, Brooks DJ, Owen D, Sharp D, Muraro PA, Gunn R, Nicholas Ret al., 2019, Confirmation of Specific Binding of the 18-kDa Translocator Protein (TSPO) Radioligand [18F]GE-180: a Blocking Study Using XBD173 in Multiple Sclerosis Normal Appearing White and Grey Matter., Mol Imaging Biol

PURPOSE: Measurements of non-displaceable binding (VND) of positron emission tomography (PET) ligands are not often made in vivo in humans because they require ligands to displace binding to target receptors and there are few readily available, safe ones to use. A technique to measure VND for ligands for the 18-kDa translocator protein (TSPO) has recently been developed which compares the total volume of distribution (VT) before and after administration of the TSPO ligand XBD173. Here, we used XBD173 with an occupancy plot to quantify VND for two TSPO radiotracers, [18F]GE-180 and [11C]PBR28, in cohorts of people with multiple sclerosis (MS). Additionally, we compared plots of subjects carrying high (HAB) or mixed binding (MAB) affinity polymorphisms of TSPO to estimate VND without receptor blockade. PROCEDURES: Twelve people with MS underwent baseline MRI and 90-min dynamic [18F]GE-180 PET or [11C]PBR28 PET (n = 6; three HAB, three MAB each). Arterial blood sampling was used to generate plasma input functions for the two-tissue compartment model. VND was calculated using two independent methods: the occupancy plot (by modelling the differences in signal post XBD173) and the polymorphism plot (by modelling the differences in signal across presence and absence of rs6971 genotypes). RESULTS: Whole brain VT (mean ± standard deviation) was 0.29 ± 0.17 ml/cm3 for [18F]GE-180 and 5.01 ± 1.88 ml/cm3 for [11C]PBR28. Using the occupancy and polymorphism plots respectively, VND for [18F]GE-180 was 0.11 ml/cm3 (95 % CI = 0.02, 0.16) and 0.20 ml/cm3 (0.16, 0.34), accounting for, on average, 55 % of VT in the whole brain. For [11C]PBR28, these values were 3.81 ml/cm3 (3.02, 4.21) and 3.49 ml/cm3 (1.38, 4.27), accounting for 67 % of average whole brain VT. CONCLUSIONS: Although VT for [18F]GE-180 is low, indicating low brain penetration, half the signal shown

JOURNAL ARTICLE

Kübler D, Wächter T, Cabanel N, Su Z, Turkheimer FE, Dodel R, Brooks DJ, Oertel WH, Gerhard Aet al., 2019, Widespread microglial activation in multiple system atrophy., Mov Disord

BACKGROUND: The pattern and role of microglial activation in multiple system atrophy is largely unclear. The objective of this study was to use [11 C](R)-PK11195 PET to determine the extent and correlation of activated microglia with clinical parameters in MSA patients. METHODS: Fourteen patients with the parkinsonian phenotype of MSA (MSA-P) with a mean disease duration of 2.9 years (range 2-5 years) were examined with [11 C](R)-PK11195 PET and compared with 10 healthy controls. RESULTS: Patients with the parkinsonian phenotype of MSA showed a significant (P ≤ 0.01) mean increase in binding potentials compared with healthy controls in the caudate nucleus, putamen, pallidum, precentral gyrus, orbitofrontal cortex, presubgenual anterior cingulate cortex, and the superior parietal gyrus. No correlations between binding potentials and clinical parameters were found. CONCLUSIONS: In early clinical stages of the parkinsonian phenotype of MSA, there is widespread microglial activation as a marker of neuroinflammatory changes without correlation to clinical parameters in our patient population. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

JOURNAL ARTICLE

Durcan R, Wiblin L, Lawson RA, Khoo TK, Yarnall AJ, Duncan GW, Brooks DJ, Pavese N, Burn DJ, ICICLE-PD Study Groupet al., 2019, Prevalence and duration of non-motor symptoms in prodromal Parkinson's disease., Eur J Neurol

BACKGROUND AND PURPOSE: The prevalence and duration of non-motor symptoms (NMS) in prodromal Parkinson's disease (PD) has not been extensively studied. The aim of this study was to determine the prevalence and duration of prodromal NMS (pNMS) in a cohort of patients with recently diagnosed PD. METHODS: We evaluated the prevalence and duration of pNMS in patients with early PD (n = 154). NMS were screened for using the Non-Motor Symptom Questionnaire (NMSQuest). We subtracted the duration of the presence of each individual NMS reported from the duration of the earliest motor symptom. NMS whose duration preceded the duration of motor symptoms were considered a pNMS. Individual pNMS were then grouped into relevant pNMS clusters based on the NMSQuest domains. Motor subtypes were defined as tremor dominant, postural instability gait difficulty (PIGD) and indeterminate type according to the Movement Disorder Society Unified Parkinson's Disease Rating Scale revision. RESULTS: Prodromal NMS were experienced by 90.3% of patients with PD and the median number experienced was 4 (interquartile range, 2-7). A gender difference existed in the pNMS experienced, with males reporting more sexual dysfunction, forgetfulness and dream re-enactment, whereas females reported more unexplained weight change and anxiety. There was a significant association between any prodromal gastrointestinal symptoms [odds ratio (OR), 2.30; 95% confidence interval (CI), 1.08-4.89, P = 0.03] and urinary symptoms (OR, 2.54; 95% CI, 1.19-5.35, P = 0.016) and the PIGD phenotype. Further analysis revealed that total pNMS were not significantly associated with the PIGD phenotype (OR, 1.10; 95% CI, 0.99-1.21, P = 0.068). CONCLUSIONS: Prodromal NMS are common and a gender difference in pNMS experienced in prodromal PD may exist. The PIGD phenotype had a higher prevalence of prodromal gastrointestinal and urinary tract symptoms.

JOURNAL ARTICLE

McGinnity CJ, Arstad E, Beck K, Brooks DJ, Coles JP, Duncan JS, Galovic M, Hinz R, Hirani E, Howes OD, Jones PA, Koepp MJ, Luo F, Barros DAR, Singh N, Trigg W, Hammers Aet 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

JOURNAL ARTICLE

Lillethorup TP, Glud AN, Landeck N, Alstrup AKO, Jakobsen S, Vang K, Doudet DJ, Brooks DJ, Kirik D, Hinz R, Sorensen JC, Landau AMet al., 2018, In vivo quantification of glial activation in minipigs overexpressing human alpha-synuclein, SYNAPSE, Vol: 72, ISSN: 0887-4476

JOURNAL ARTICLE

Sridharan S, Raffel J, Nandoskar A, Record C, Brooks D, Owen D, Sharp D, Muraro P, Gunn R, Nicholas Ret 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

CONFERENCE PAPER

Parbo P, Ismail R, Sommerauer M, Stokholm MG, Hansen AK, Hansen KV, Amidi A, Schaldemose JL, Gottrup H, Braendgaard H, Eskildsen SF, Borghammer P, Hinz R, Aanerud J, Brooks DJet 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

JOURNAL ARTICLE

Dani M, Wood M, Mizoguchi R, Fan Z, Walker Z, Morgan R, Hinz R, Biju M, Kuruvilla T, Brooks DJ, Edison Pet 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

JOURNAL ARTICLE

Calsolaro V, Fan Z, Veronese M, Femminella G, Pasqualetti G, Trigg W, Buckley C, Turkheimer F, Gentleman S, Hinz R, Brooks D, Edison Pet 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

JOURNAL ARTICLE

Femminella G, Fan Z, Frangou E, Love S, Calsolaro V, Holmes C, Ritchie C, Lawrence R, McFarlane B, Tadros G, Ridha B, Bannister C, Walker Z, Archer H, Coulthard E, Underwood B, Prasanna A, Korentang P, Karim S, Junaid K, McGuinness B, Passmore P, Nilforooshan R, Macharouthu A, Donaldson A, Thacker S, Russell G, Malik N, Mate V, Knight L, Kshemendran S, Harrison J, Ballard C, Brooks D, Edison Pet 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

JOURNAL ARTICLE

Mattsson N, Groot C, Jansen WJ, Landau SM, Villemagne VL, Engelborghs S, Mintun MM, Lleo A, Molinuevo JL, Jagust WJ, Frisoni GB, Ivanoiu A, Chetelat G, de Oliveira CR, Rodrigue KM, Kornhuber J, Wallin A, Klimkowicz-Mrowiec A, Kandimalla R, Popp J, Aalten PP, Aarsland D, Alcolea D, Almdahl IS, Baldeiras I, van Buchem MA, Cavedo E, Chen K, Cohen AD, Foerster S, Fortea J, Frederiksen KS, Freund-Levi Y, Gill KD, Gkatzima O, Grimmer T, Hampel H, Herukka S-K, Johannsen P, van Laere K, de Leon MJ, Maier W, Marcusson J, Meulenbroek O, Mollergard HM, Morris JC, Mroczko B, Nordlund A, Prabhakar S, Peters O, Rami L, Rodriguez-Rodriguez E, Roe CM, Ruther E, Santana I, Schroder J, Seo SW, Soininen H, Spiru L, Stomrud E, Struyfs H, Teunissen CE, Verhey FRJ, Vos SJB, van Doorn LJCVW, Waldemar G, Wallin AK, Wiltfang J, Vandenberghe R, Brooks DJ, Fladby T, Rowe CC, Drzezga A, Verbeek MM, Sarazin M, Wolk DA, Fleisher AS, Klunk WE, Na DL, Sanchez-Juan P, Lee DY, Nordberg A, Tsolaki M, Camus V, Rinne JO, Fagan AM, Zetterberg H, Blennow K, Rabinovici GD, Hansson O, van Berckel BNM, van der Flier WM, Scheltens P, Visser PJ, Ossenkoppele Ret 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

JOURNAL ARTICLE

Fan Z, Dani M, Femminella GD, Wood M, Calsolaro V, Veronese M, Turkheimer F, Gentleman S, Brooks DJ, Hinz R, Edison Pet 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

JOURNAL ARTICLE

Minett T, Su L, Mak E, Williams G, Firbank M, Lawson RA, Yarnall AJ, Duncan GW, Owen AM, Khoo TK, Brooks DJ, Rowe JB, Barker RA, Burn D, O'Brien JTet 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

JOURNAL ARTICLE

Stokholm MG, Iranzo A, Ostergaard K, Serradell M, Otto M, Svendsen KB, Garrido A, Vilas D, Parbo P, Borghammer P, Santamaria J, Moller A, Gaig C, Brooks DJ, Tolosa E, Pavese Net 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

JOURNAL ARTICLE

Knudsen K, Fedorova TD, Hansen AK, Sommerauer M, Otto M, Svendsen KB, Nahimi A, Stokholm MG, Pavese N, Beier CP, Brooks DJ, Borghammer Pet 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

JOURNAL ARTICLE

McGinnity CJ, Barros DAR, Trigg W, Brooks DJ, Hinz R, Duncan JS, Koepp MJ, Hammers Aet 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

JOURNAL ARTICLE

Sommerauer M, Hansen AK, Parbo P, Fedorova TD, Knudsen K, Frederiksen Y, Nahimi A, Barbe MT, Brooks DJ, Borghammer Pet 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

JOURNAL ARTICLE

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

JOURNAL ARTICLE

Lillethorup TP, Glud AN, Alstrup AKO, Mikkelsen TW, Nielsen EH, Zaer H, Doudet DJ, Brooks DJ, Sorensen JCH, Orlowski D, Landau AMet al., 2018, Nigrostriatal proteasome inhibition impairs dopamine neurotransmission and motor function in minipigs, EXPERIMENTAL NEUROLOGY, Vol: 303, Pages: 142-152, ISSN: 0014-4886

JOURNAL ARTICLE

Pasquini J, Ceravolo R, Qamhawi Z, Lee J-Y, Deuschl G, Brooks DJ, Bonuccelli U, Pavese Net 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

JOURNAL ARTICLE

Jeppesen J, Otto M, Frederiksen Y, Hansen AK, Fedorova TD, Knudsen K, Nahimi A, Brooks DJ, Borghammer P, Sommerauer Met 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

JOURNAL ARTICLE

Sommerauer M, Fedorova TD, Hansen AK, Knudsen K, Otto M, Jeppesen J, Frederiksen Y, Blicher JU, Geday J, Nahimi A, Damholdt MF, Brooks DJ, Borghammer Pet 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

JOURNAL ARTICLE

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

JOURNAL ARTICLE

Jansen WJ, Ossenkoppele R, Tijms BM, Fagan AM, Hansson O, Klunk WE, van der Flier WM, Villemagne VL, Frisoni GB, Fleisher AS, Lleo A, Mintun MA, Wallin A, Engelborghs S, Na DL, Chetelat G, Molinuevo JL, Landau SM, Mattsson N, Kornhuber J, Sabri O, Rowe CC, Parnetti L, Popp J, Fladby T, Jagust WJ, Aalten P, Lee DY, Vandenberghe R, de Oliveira CR, Kapaki E, Froelich L, Ivanoiu A, Gabryelewicz T, Verbeek MM, Sanchez-Juan P, Hildebrandt H, Camus V, Zboch M, Brooks DJ, Drzezga A, Rinne JO, Newberg A, de Mendonca A, Sarazin M, Rabinovici GD, Madsen K, Kramberger MG, Nordberg A, Mok V, Mroczko B, Wolk DA, Meyer PT, Tsolaki M, Scheltens P, Verhey FRJ, Visser PJet 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

JOURNAL ARTICLE

Ismail R, Hansen AK, Parbo P, Brændgaard H, Gottrup H, Brooks DJ, Borghammer Pet 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.

JOURNAL ARTICLE

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