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3. Cuneus atrophy and Parkinsonian phenoconversion in cognitively unimpaired patients with isolated REM sleep behavior disorder

Author

Baun, Andreas Myhre, Iranzo, Alex, Terkelsen, Miriam Højholt, Stokholm, Morten Gersel, Stær, Kristian, Serradell, Mónica, Otto, Marit, Svendsen, Kristina Bacher, Garrido, Alicia, Vilas, Dolores, Santamaria, Joan, Møller, Arne, Gaig, Carles, Brooks, David J., Borghammer, Per, Tolosa, Eduardo, Eskildsen, Simon Fristed, and Pavese, Nicola

Published
2025
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4. Amyloid-β aggregates activate peripheral monocytes in mild cognitive impairment

Author

Juul-Madsen, Kristian, Parbo, Peter, Ismail, Rola, Ovesen, Peter L., Schmidt, Vanessa, Madsen, Lasse S., Thyrsted, Jacob, Gierl, Sarah, Breum, Mihaela, Larsen, Agnete, Andersen, Morten N., Romero-Ramos, Marina, Holm, Christian K., Andersen, Gregers R., Zhao, Huaying, Schuck, Peter, Nygaard, Jens V., Sutherland, Duncan S., Eskildsen, Simon F., Willnow, Thomas E., Brooks, David J., and Vorup-Jensen, Thomas

Published
2024
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15. Spontaneous partial recovery of striatal dopaminergic uptake despite nigral cell loss in asymptomatic MPTP-lesioned female minipigs

Author

Lillethorup, Thea P., Noer, Ove, Alstrup, Aage Kristian Olsen, Real, Caroline C., Stokholm, Kathrine, Thomsen, Majken Borup, Zaer, Hamed, Orlowski, Dariusz, Mikkelsen, Trine Werenberg, Glud, Andreas N., Nielsen, Erik Holm Toustrup, Schacht, Anna C., Winterdahl, Michael, Brooks, David J., Sørensen, Jens Christian H., and Landau, Anne M.

Published
2022
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16. Cholinergic dysfunction in isolated rapid eye movement sleep behaviour disorder links to impending phenoconversion.

Author

Terkelsen, Miriam H., Iranzo, Alex, Serradell, Mónica, Baun, Andreas M., Stokholm, Morten G., Danielsen, Erik Hvid, Østergaard, Karen, Otto, Marit, Svendsen, Kristina B., Møller, Mette, Johnsen, Erik L., Garrido, Alicia, Vilas, Dolores, Santamaria, Joan, Møller, Arne, Gaig, Carles, Brooks, David J., Borghammer, Per, Tolosa, Eduardo, and Pavese, Nicola

Subjects
DOPAMINERGIC imaging, RAPID eye movement sleep, LEWY body dementia, SLEEP, POSITRON emission tomography
Abstract

Background and purpose: Most patients with isolated rapid eye movement sleep behaviour disorder (iRBD) progress to a parkinsonian alpha‐synucleinopathy. However, time to phenoconversion shows great variation. The aim of this study was to investigate whether cholinergic and dopaminergic dysfunction in iRBD patients was associated with impending phenoconversion. Methods: Twenty‐one polysomnography‐confirmed iRBD patients underwent baseline 11C‐donepezil and 6‐Fluoro‐(18F)‐l‐3,4‐dihydroxyphenylalanine (18F‐DOPA) positron emission tomography (PET). Potential phenoconversion was monitored for up to 8 years. PET images were analysed according to patients' diagnoses after 3 and 8 years using linear regression. Time‐to‐event analysis was made with Cox regression, dividing patients into low and high tracer uptake groups. Results: Follow‐up was accomplished in 17 patients. Eight patients progressed to either Parkinson's disease (n = 4) or dementia with Lewy bodies (n = 4), while nine remained non‐phenoconverters. Compared with non‐phenoconverters, 8‐year phenoconverters had lower mean 11C‐donepezil uptake in the parietal (p = 0.032) and frontal cortex (p = 0.042), whereas mean 11C‐donepezil uptake in 3‐year phenoconverters was lower in the parietal cortex (p = 0.005), frontal cortex (p = 0.025), thalamus (p = 0.043) and putamen (p = 0.049). Phenoconverters within 3 years and 8 years had lower 18F‐DOPA uptake in the putamen (p < 0.001). iRBD patients with low parietal 11C‐donepezil uptake had a 13.46 (95% confidence interval 1.42;127.21) times higher rate of phenoconversion compared with those with higher uptake (p = 0.023). iRBD patients with low 18F‐DOPA uptake in the most affected putamen were all phenoconverters with higher rate of phenoconversion (p = 0.0002). Conclusions: These findings suggest that cortical cholinergic dysfunction, particularly within the parietal cortex, could be a biomarker candidate for predicting short‐term phenoconversion in iRBD patients. This study aligns with previous reports suggesting dopaminergic dysfunction is associated with forthcoming phenoconversion. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Microglial responses partially mediate the effect of Aβ on cognition in Alzheimer's disease.

Author

Madsen, Lasse S., Ismail, Rola, Parbo, Peter, Kjeldsen, Pernille L., Schaldemose, Jeppe L., Hansen, Kim V., Gottrup, Hanne, Aanerud, Joel, Eskildsen, Simon F., and Brooks, David J.

Abstract

INTRODUCTION: Microglial responses are an integral part of Alzheimer's disease (AD) pathology and are associated with amyloid beta (Aβ) deposition. This study aimed to investigate the effects of Aβ and microglial responses on global cognitive impairment. METHODS: In this longitudinal study, 28 patients with mild cognitive impairment and 11 healthy controls underwent 11C‐PK11195 and 11C‐Pittsburgh compound B positron emission tomography (PET), structural magnetic resonance imaging scans, and global cognitive ratings at baseline and 2‐year follow‐up. Correlations between PET uptake and global cognition were assessed. Additionally, the mediation effect of the microglial response on the association between Aβ load and global cognition was assessed. RESULTS: Aβ load and the microglial response were both independently detrimental to global cognitive performance at baseline; however, at 2‐year follow‐up the association between Aβ load and global cognitive ratings was partially mediated by the microglial response. DISCUSSION: As AD progresses, the associated microglial response partially mediates the detrimental effect of aggregated Aβ on cognition. Highlights: This was a longitudinal study of amyloid beta (Aβ), microglial responses, and global cognitive performance.Aβ and microglial responses both affect cognition in early Alzheimer's disease.Microglial response partially mediates the effect of Aβ on cognition in later stages. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Combined Neuroinflammation and Amyloid PET Markers in Predicting Disease Progression in Cognitively Impaired Subjects.

Author

Leng, Fangda, Hinz, Rainer, Gentleman, Steve, Dani, Melanie, Brooks, David J., and Edison, Paul

Subjects
POSITRON emission tomography, MILD cognitive impairment, ALZHEIMER'S disease, PROGNOSIS, DISEASE progression
Abstract

Background: Neuroinflammation in Alzheimer's disease is known as an important process in the disease, yet how microglial activation affects disease progression remains unclear. Objective: The current study aims to interrogate the predictive value of neuroinflammation biomarker (11C-PBR28 PET), together with A/T/N imaging markers on disease deterioration in a cognitively impaired patient cohort. Methods: The study included 6 AD and 27 MCI patients, who had MRI, 11C-PBR28, 18F-flutemetamol (amyloid marker), 18F-AV1451 (tau marker) PET scans, and were followed up with multiple neuropsychological assessments for at least one year (1.6 and 2.8 years on average for AD and MCI). The predictive values of imaging biomarkers on baseline and longitudinal cognition were interrogated using linear regression to identify the biomarkers that could explain disease progression. Results: Linear mixed models found the average intercepts (baseline) MMSE were 23.5 for AD and 28.2 for MCI patients, and the slope of MMSE (annual change) were –0.74 for AD and –0.52 for MCI patients. White matter microstructural integrity was predictive of baseline cognition, while PET markers of amyloid, tau and neuroinflammation were predictive of longitudinal cognitive decline. Both amyloid and neuroinflammation PET markers were predictors independent of each other. And a sub-group analysis showed the predictive effect of neuroinflammation on cognitive decline is independent of amyloid and tau. Conclusions: Our study highlights the prognostic value of disease specific markers (amyloid, tau and neuroinflammation) in clinically diagnosed AD and MCI patients and suggests that the effects of these molecular markers are mediated by structural damage to the brain. [ABSTRACT FROM AUTHOR]

Published
2024
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27. Microglial Activation and Progression of Nigrostriatal Dysfunction in Isolated REM Sleep Behavior Disorder.

Author

Stær, Kristian, Iranzo, Alex, Stokholm, Morten Gersel, Hvingelby, Victor S., Danielsen, Erik Hvid, Østergaard, Karen, Serradell, Mónica, Otto, Marit, Svendsen, Kristina B., Garrido, Alicia, Vilas, Dolores, Santamaria, Joan, Møller, Arne, Gaig, Carles, Brooks, David J., Borghammer, Per, Tolosa, Eduardo, and Pavese, Nicola

Abstract

Background: Using 11C‐(R)‐PK11195‐PET, we found increased microglia activation in isolated REM sleep behavior disorder (iRBD) patients. Their role remains to be clarified. Objectives: The objective is to assess relationships between activated microglia and progression of nigrostriatal dysfunction in iRBD. Methods: Fifteen iRBD patients previously scanned with 11C‐(R)‐PK11195 and 18F‐DOPA‐PET underwent repeat 18F‐DOPA‐PET after 3 years. 18F‐DOPA Ki changes from baseline were evaluated with volumes‐of‐interest and voxel‐based analyses. Results: Significant 18F‐DOPA Ki reductions were found in putamen and caudate. Reductions were larger and more widespread in patients with increased nigral microglia activation at baseline. Left nigral 11C‐(R)‐PK11195 binding at baseline was a predictor of 18F‐DOPA Ki reduction in left caudate (coef = −0.0426, P = 0.016). Conclusions: Subjects with increased baseline 11C‐(R)‐PK11195 binding have greater changes in nigrostriatal function, suggesting a detrimental rather than protective effect of microglial activation. Alternatively, both phenomena occur in patients with prominent nigrostriatal dysfunction without a causative link. The clinical and therapeutic implications of these findings need further elucidation. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Published
2024
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29. Amyloid-PET and 18F-FDG-PET in the diagnostic investigation of Alzheimer's disease and other dementias

Author

Chételat, Gaël, Arbizu, Javier, Barthel, Henryk, Garibotto, Valentina, Law, Ian, Morbelli, Silvia, van de Giessen, Elsmarieke, Agosta, Federica, Barkhof, Frederik, Brooks, David J, Carrillo, Maria C, Dubois, Bruno, Fjell, Anders M, Frisoni, Giovanni B, Hansson, Oskar, Herholz, Karl, Hutton, Brian F, Jack, Clifford R, Jr, Lammertsma, Adriaan A, Landau, Susan M, Minoshima, Satoshi, Nobili, Flavio, Nordberg, Agneta, Ossenkoppele, Rik, Oyen, Wim J G, Perani, Daniela, Rabinovici, Gil D, Scheltens, Philip, Villemagne, Victor L, Zetterberg, Henrik, and Drzezga, Alexander

Published
2020
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34. EANM practice guideline/SNMMI procedure standard for dopaminergic imaging in Parkinsonian syndromes 1.0

Author

Morbelli, Silvia, Esposito, Giuseppe, Arbizu, Javier, Barthel, Henryk, Boellaard, Ronald, Bohnen, Nico I., Brooks, David J, Darcourt, Jacques, Dickson, John C., Douglas, David, Drzezga, Alexander, Dubroff, Jacob, Ekmekcioglu, Ozgul, Garibotto, Valentina, Herscovitch, Peter, Kuo, Phillip, Lammertsma, Adriaan, Pappata, Sabina, Peñuelas, Iván, Seibyl, John, Semah, Franck, Tossici-Bolt, Livia, Van de Giessen, Elsmarieke, Van Laere, Koen, Varrone, Andrea, Wanner, Michele, Zubal, George, and Law, Ian

Published
2020
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36. Does insulin resistance influence neurodegeneration in non-diabetic Alzheimer’s subjects?

Author

Femminella, Grazia Daniela, Livingston, Nicholas R., Raza, Sanara, van der Doef, Thalia, Frangou, Eleni, Love, Sharon, Busza, Gail, Calsolaro, Valeria, Carver, Stefan, Holmes, Clive, Ritchie, Craig W., Lawrence, Robert M., McFarlane, Brady, Tadros, George, Ridha, Basil H., Bannister, Carol, Walker, Zuzana, Archer, Hilary, Coulthard, Elizabeth, Underwood, Ben, Prasanna, Aparna, Koranteng, Paul, Karim, Salman, Junaid, Kehinde, McGuinness, Bernadette, Passmore, Anthony Peter, Nilforooshan, Ramin, Macharouthu, Ajayverma, Donaldson, Andrew, Thacker, Simon, Russell, Gregor, Malik, Naghma, Mate, Vandana, Knight, Lucy, Kshemendran, Sajeev, Tan, Tricia, Holscher, Christian, Harrison, John, Brooks, David J., Ballard, Clive, and Edison, Paul

Published
2021
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37. Subanesthetic S‐ketamine does not acutely alter striatal dopamine transporter binding in healthy Sprague Dawley female rats.

Author

Bærentzen, Simone Larsen, Thomsen, Jakob Borup, Thomsen, Majken Borup, Jakobsen, Steen, Simonsen, Mette Theilgaard, Wegener, Gregers, Brooks, David J., and Landau, Anne M.

Subjects
DOPAMINERGIC imaging, POSITRON emission tomography, MENTAL depression, SPRAGUE Dawley rats, MENTAL illness
Abstract

Major depressive disorder is one of the most prevalent mental health disorders, posing a global socioeconomic burden. Conventional antidepressant treatments have a slow onset of action, and 30% of patients show no clinically significant treatment response. The recently approved fast‐acting antidepressant S‐ketamine, an N‐methyl‐D‐aspartate receptor antagonist, provides a new approach for treatment‐resistant patients. However, knowledge of S‐ketamine's mechanism of action is still being established. Depressed human subjects have lower striatal dopamine transporter (DAT) availability compared to healthy controls. Rodent studies report increased striatal dopamine concentration in response to acute ketamine administration. In vivo [18F]FE‐PE2I ([18F]‐(E)‐N‐(3‐iodoprop‐2‐enyl)‐2β‐carbofluoroethoxy‐3β‐(4′‐methyl‐phenyl) nortropane) positron emission tomography (PET) imaging of the DAT has not previously been applied to assess the effect of acute subanesthetic S‐ketamine administration on DAT availability. We applied translational in vivo [18F]FE‐PE2I PET imaging of the DAT in healthy female rats to evaluate whether an acute subanesthetic intraperitoneal dose of 15 mg/kg S‐ketamine alters DAT availability. We also performed [3H]GBR‐12935 autoradiography on postmortem brain sections. We found no effect of acute S‐ketamine administration on striatal DAT binding using [18F]FE‐PE2I PET or [3H]GBR‐12935 autoradiography. This negative result does not support the hypothesis that DAT changes are associated with S‐ketamine's rapid antidepressant effects, but additional studies are warranted. [ABSTRACT FROM AUTHOR]

Published
2024
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39. Prevalence of the apolipoprotein E ε4 allele in amyloid β positive subjects across the spectrum of Alzheimer's disease

Author

Mattsson, Niklas, Groot, Colin, Jansen, Willemijn J., Landau, Susan M., Villemagne, Victor L., Engelborghs, Sebastiaan, Mintun, Mark M., Lleo, Alberto, Molinuevo, José Luis, Jagust, William J., Frisoni, Giovanni B., Ivanoiu, Adrian, Chételat, Gaël, Resende de Oliveira, Catarina, Rodrigue, Karen M., Kornhuber, Johannes, Wallin, Anders, Klimkowicz-Mrowiec, Aleksandra, Kandimalla, Ramesh, Popp, Julius, Aalten, Pauline P., Aarsland, Dag, Alcolea, Daniel, Almdahl, Ina S., Baldeiras, Inês, van Buchem, Mark A., Cavedo, Enrica, Chen, Kewei, Cohen, Ann D., Förster, Stefan, Fortea, Juan, Frederiksen, Kristian S., Freund-Levi, Yvonne, Gill, Kiran Dip, Gkatzima, Olymbia, Grimmer, Timo, Hampel, Harald, Herukka, Sanna-Kaisa, Johannsen, Peter, van Laere, Koen, de Leon, Mony J., Maier, Wolfgang, Marcusson, Jan, Meulenbroek, Olga, Møllergård, Hanne M., Morris, John C., Mroczko, Barbara, Nordlund, Arto, Prabhakar, Sudesh, Peters, Oliver, Rami, Lorena, Rodríguez-Rodríguez, Eloy, Roe, Catherine M., Rüther, Eckart, Santana, Isabel, Schröder, Johannes, Seo, Sang W., Soininen, Hilkka, Spiru, Luiza, Stomrud, Erik, Struyfs, Hanne, Teunissen, Charlotte E., Verhey, Frans R.J., Vos, Stephanie J.B., van Waalwijk van Doorn, Linda J.C., Waldemar, Gunhild, Wallin, Åsa K., Wiltfang, Jens, Vandenberghe, Rik, Brooks, David J., Fladby, Tormod, Rowe, Christopher C., Drzezga, Alexander, Verbeek, Marcel M., Sarazin, Marie, Wolk, David A., Fleisher, Adam S., Klunk, William E., Na, Duk L., Sánchez-Juan, Pascual, Lee, Dong Young, Nordberg, Agneta, Tsolaki, Magda, Camus, Vincent, Rinne, Juha O., Fagan, Anne M., Zetterberg, Henrik, Blennow, Kaj, Rabinovici, Gil D., Hansson, Oskar, van Berckel, Bart N.M., van der Flier, Wiesje M., Scheltens, Philip, Visser, Pieter Jelle, and Ossenkoppele, Rik

Published
2018
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