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3. Beyond the symptom: the biology of fatigue.

Author

Raizen, David, Mullington, Janet, Anaclet, Christelle, Clarke, Gerard, Critchley, Hugo, Dantzer, Robert, Davis, Ronald, Drew, Kelly, Fessel, Josh, Fuller, Patrick, Gibson, Erin, Harrington, Mary, Ian Lipkin, W, Klerman, Elizabeth, Klimas, Nancy, Komaroff, Anthony, Koroshetz, Walter, Krupp, Lauren, Kuppuswamy, Anna, Lasselin, Julie, Lewis, Laura, Magistretti, Pierre, Matos, Heidi, Miaskowski, Christine, Miller, Andrew, Nath, Avindra, Nedergaard, Maiken, Opp, Mark, Ritchie, Marylyn, Rogulja, Dragana, Rolls, Asya, Salamone, John, Saper, Clifford, Whittemore, Vicky, Wylie, Glenn, Younger, Jarred, Zee, Phyllis, and Craig Heller, H

Subjects
Humans, Fatigue, Motivation, Biology
Abstract

A workshop titled Beyond the Symptom: The Biology of Fatigue was held virtually September 27-28, 2021. It was jointly organized by the Sleep Research Society and the Neurobiology of Fatigue Working Group of the NIH Blueprint Neuroscience Research Program. For access to the presentations and video recordings, see: https://neuroscienceblueprint.nih.gov/about/event/beyond-symptom-biology-fatigue. The goals of this workshop were to bring together clinicians and scientists who use a variety of research approaches to understand fatigue in multiple conditions and to identify key gaps in our understanding of the biology of fatigue. This workshop summary distills key issues discussed in this workshop and provides a list of promising directions for future research on this topic. We do not attempt to provide a comprehensive review of the state of our understanding of fatigue, nor to provide a comprehensive reprise of the many excellent presentations. Rather, our goal is to highlight key advances and to focus on questions and future approaches to answering them.

Published
2023

16. Lactate biosensors for spectrally and spatially multiplexed fluorescence imaging

Author

Nasu, Yusuke, Aggarwal, Abhi, Le, Giang N. T., Vo, Camilla Trang, Kambe, Yuki, Wang, Xinxing, Beinlich, Felix R. M., Lee, Ashley Bomin, Ram, Tina R., Wang, Fangying, Gorzo, Kelsea A., Kamijo, Yuki, Boisvert, Marc, Nishinami, Suguru, Kawamura, Genki, Ozawa, Takeaki, Toda, Hirofumi, Gordon, Grant R., Ge, Shaoyu, Hirase, Hajime, Nedergaard, Maiken, Paquet, Marie-Eve, Drobizhev, Mikhail, Podgorski, Kaspar, and Campbell, Robert E.

Published
2023
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26. A community-based transcriptomics classification and nomenclature of neocortical cell types

Author

Yuste, Rafael, Hawrylycz, Michael, Aalling, Nadia, Aguilar-Valles, Argel, Arendt, Detlev, Armañanzas, Ruben, Ascoli, Giorgio A, Bielza, Concha, Bokharaie, Vahid, Bergmann, Tobias Borgtoft, Bystron, Irina, Capogna, Marco, Chang, YoonJeung, Clemens, Ann, de Kock, Christiaan PJ, DeFelipe, Javier, Dos Santos, Sandra Esmeralda, Dunville, Keagan, Feldmeyer, Dirk, Fiáth, Richárd, Fishell, Gordon James, Foggetti, Angelica, Gao, Xuefan, Ghaderi, Parviz, Goriounova, Natalia A, Güntürkün, Onur, Hagihara, Kenta, Hall, Vanessa Jane, Helmstaedter, Moritz, Herculano-Houzel, Suzana, Hilscher, Markus M, Hirase, Hajime, Hjerling-Leffler, Jens, Hodge, Rebecca, Huang, Josh, Huda, Rafiq, Khodosevich, Konstantin, Kiehn, Ole, Koch, Henner, Kuebler, Eric S, Kühnemund, Malte, Larrañaga, Pedro, Lelieveldt, Boudewijn, Louth, Emma Louise, Lui, Jan H, Mansvelder, Huibert D, Marin, Oscar, Martinez-Trujillo, Julio, Chameh, Homeira Moradi, Mohapatra, Alok Nath, Munguba, Hermany, Nedergaard, Maiken, Němec, Pavel, Ofer, Netanel, Pfisterer, Ulrich Gottfried, Pontes, Samuel, Redmond, William, Rossier, Jean, Sanes, Joshua R, Scheuermann, Richard H, Serrano-Saiz, Esther, Staiger, Jochen F, Somogyi, Peter, Tamás, Gábor, Tolias, Andreas Savas, Tosches, Maria Antonietta, García, Miguel Turrero, Wozny, Christian, Wuttke, Thomas V, Liu, Yong, Yuan, Juan, Zeng, Hongkui, and Lein, Ed

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Biotechnology, Genetics, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Animals, Cells, Computational Biology, Humans, Neocortex, Neuroglia, Neurons, Single-Cell Analysis, Terminology as Topic, Transcriptome, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

To understand the function of cortical circuits, it is necessary to catalog their cellular diversity. Past attempts to do so using anatomical, physiological or molecular features of cortical cells have not resulted in a unified taxonomy of neuronal or glial cell types, partly due to limited data. Single-cell transcriptomics is enabling, for the first time, systematic high-throughput measurements of cortical cells and generation of datasets that hold the promise of being complete, accurate and permanent. Statistical analyses of these data reveal clusters that often correspond to cell types previously defined by morphological or physiological criteria and that appear conserved across cortical areas and species. To capitalize on these new methods, we propose the adoption of a transcriptome-based taxonomy of cell types for mammalian neocortex. This classification should be hierarchical and use a standardized nomenclature. It should be based on a probabilistic definition of a cell type and incorporate data from different approaches, developmental stages and species. A community-based classification and data aggregation model, such as a knowledge graph, could provide a common foundation for the study of cortical circuits. This community-based classification, nomenclature and data aggregation could serve as an example for cell type atlases in other parts of the body.

Published
2020

27. A community-based transcriptomics classification and nomenclature of neocortical cell types

Author

Yuste, Rafael, Hawrylycz, Michael, Aalling, Nadia, Arendt, Detlev, Armananzas, Ruben, Ascoli, Giorgio, Bielza, Concha, Bokharaie, Vahid, Bergmann, Tobias, Bystron, Irina, Capogna, Marco, Chang, Yoonjeung, Clemens, Ann, de Kock, Christiaan, DeFelipe, Javier, Santos, Sandra Dos, Dunville, Keagan, Feldmeyer, Dirk, Fiath, Richard, Fishell, Gordon, Foggetti, Angelica, Gao, Xuefan, Ghaderi, Parviz, Gunturkun, Onur, Hall, Vanessa Jane, Helmstaedter, Moritz, Herculano-Houzel, Suzana, Hilscher, Markus, Hirase, Hajime, Hjerling-Leffler, Jens, Hodge, Rebecca, Huang, Z. Josh, Huda, Rafiq, Juan, Yuan, Khodosevich, Konstantin, Kiehn, Ole, Koch, Henner, Kuebler, Eric, Kuhnemund, Malte, Larranaga, Pedro, Lelieveldt, Boudewijn, Louth, Emma Louise, Lui, Jan, Mansvelder, Huibert, Marin, Oscar, Martínez-Trujillo, Julio, Moradi, Homeira, Goriounova, Natalia, Mohapatra, Alok, Nedergaard, Maiken, Němec, Pavel, Ofer, Netanel, Pfisterer, Ulrich, Pontes, Samuel, Redmond, William, Rossier, Jean, Sanes, Joshua, Scheuermann, Richard, Saiz, Esther Serrano, Somogyi, Peter, Tamás, Gábor, Tolias, Andreas, Tosches, Maria, Garcia, Miguel Turrero, Aguilar-Valles, Argel, Munguba, Hermany, Wozny, Christian, Wuttke, Thomas, Yong, Liu, Zeng, Hongkui, and Lein, Ed S.

Subjects
Quantitative Biology - Genomics, Quantitative Biology - Neurons and Cognition
Abstract

To understand the function of cortical circuits it is necessary to classify their underlying cellular diversity. Traditional attempts based on comparing anatomical or physiological features of neurons and glia, while productive, have not resulted in a unified taxonomy of neural cell types. The recent development of single-cell transcriptomics has enabled, for the first time, systematic high-throughput profiling of large numbers of cortical cells and the generation of datasets that hold the promise of being complete, accurate and permanent. Statistical analyses of these data have revealed the existence of clear clusters, many of which correspond to cell types defined by traditional criteria, and which are conserved across cortical areas and species. To capitalize on these innovations and advance the field, we, the Copenhagen Convention Group, propose the community adopts a transcriptome-based taxonomy of the cell types in the adult mammalian neocortex. This core classification should be ontological, hierarchical and use a standardized nomenclature. It should be configured to flexibly incorporate new data from multiple approaches, developmental stages and a growing number of species, enabling improvement and revision of the classification. This community-based strategy could serve as a common foundation for future detailed analysis and reverse engineering of cortical circuits and serve as an example for cell type classification in other parts of the nervous system and other organs., Comment: 21 pages, 3 figures

Published
2019

28. An ocular glymphatic clearance system removes β-amyloid from the rodent eye

Author

Wang, Xiaowei, Lou, Nanhong, Eberhardt, Allison, Yang, Yujia, Kusk, Peter, Xu, Qiwu, Förstera, Benjamin, Peng, Sisi, Shi, Meng, Ladrón-de-Guevara, Antonio, Delle, Christine, Sigurdsson, Björn, Xavier, Anna LR, Ertürk, Ali, Libby, Richard T, Chen, Lu, Thrane, Alexander S, and Nedergaard, Maiken

Subjects
Neurosciences, Neurodegenerative, Eye Disease and Disorders of Vision, Aging, Eye, Amyloid beta-Peptides, Animals, Aquaporin 4, Glymphatic System, Intracranial Pressure, Mice, Optic Nerve, Retina, Vitreous Body, Biological Sciences, Medical and Health Sciences
Abstract

Despite high metabolic activity, the retina and optic nerve head lack traditional lymphatic drainage. We here identified an ocular glymphatic clearance route for fluid and wastes via the proximal optic nerve in rodents. β-amyloid (Aβ) was cleared from the retina and vitreous via a pathway dependent on glial water channel aquaporin-4 (AQP4) and driven by the ocular-cranial pressure difference. After traversing the lamina barrier, intra-axonal Aβ was cleared via the perivenous space and subsequently drained to lymphatic vessels. Light-induced pupil constriction enhanced efflux, whereas atropine or raising intracranial pressure blocked efflux. In two distinct murine models of glaucoma, Aβ leaked from the eye via defects in the lamina barrier instead of directional axonal efflux. The results suggest that, in rodents, the removal of fluid and metabolites from the intraocular space occurs through a glymphatic pathway that might be impaired in glaucoma.

Published
2020

32. Glymphatic System

Author

Benveniste, Helene, Nedergaard, Maiken, Pfaff, Donald W., editor, Volkow, Nora D., editor, and Rubenstein, John L., editor

Published
2022
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37. Oxygen tension-mediated erythrocyte membrane interactions regulate cerebral capillary hyperemia.

Author

Zhou, Sitong, Giannetto, Michael, DeCourcey, James, Kang, Hongyi, Kang, Ning, Li, Yizeng, Zheng, Suilan, Zhao, Hetince, Simmons, William R, Wei, Helen S, Bodine, David M, Low, Philip S, Nedergaard, Maiken, and Wan, Jiandi

Subjects
Brain, Erythrocyte Membrane, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Hyperemia, Oxygen, Anion Exchange Protein 1, Erythrocyte, Hemoglobins, Blood Flow Velocity, Cerebrovascular Circulation, Lab-On-A-Chip Devices, Clinical Research, Neurosciences, Aetiology, Underpinning research, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning
Abstract

The tight coupling between cerebral blood flow and neural activity is a key feature of normal brain function and forms the basis of functional hyperemia. The mechanisms coupling neural activity to vascular responses, however, remain elusive despite decades of research. Recent studies have shown that cerebral functional hyperemia begins in capillaries, and red blood cells (RBCs) act as autonomous regulators of brain capillary perfusion. RBCs then respond to local changes of oxygen tension (PO2) and regulate their capillary velocity. Using ex vivo microfluidics and in vivo two-photon microscopy, we examined RBC capillary velocity as a function of PO2 and showed that deoxygenated hemoglobin and band 3 interactions on RBC membrane are the molecular switch that responds to local PO2 changes and controls RBC capillary velocity. Capillary hyperemia can be controlled by manipulating RBC properties independent of the neurovascular unit, providing an effective strategy to treat or prevent impaired functional hyperemia.

Published
2019

38. Vascular dysfunction-The disregarded partner of Alzheimer's disease.

Author

Sweeney, Melanie D, Montagne, Axel, Sagare, Abhay P, Nation, Daniel A, Schneider, Lon S, Chui, Helena C, Harrington, Michael G, Pa, Judy, Law, Meng, Wang, Danny JJ, Jacobs, Russell E, Doubal, Fergus N, Ramirez, Joel, Black, Sandra E, Nedergaard, Maiken, Benveniste, Helene, Dichgans, Martin, Iadecola, Costantino, Love, Seth, Bath, Philip M, Markus, Hugh S, Salman, Rustam A, Allan, Stuart M, Quinn, Terence J, Kalaria, Rajesh N, Werring, David J, Carare, Roxana O, Touyz, Rhian M, Williams, Steve CR, Moskowitz, Michael A, Katusic, Zvonimir S, Lutz, Sarah E, Lazarov, Orly, Minshall, Richard D, Rehman, Jalees, Davis, Thomas P, Wellington, Cheryl L, González, Hector M, Yuan, Chun, Lockhart, Samuel N, Hughes, Timothy M, Chen, Christopher LH, Sachdev, Perminder, O'Brien, John T, Skoog, Ingmar, Pantoni, Leonardo, Gustafson, Deborah R, Biessels, Geert Jan, Wallin, Anders, Smith, Eric E, Mok, Vincent, Wong, Adrian, Passmore, Peter, Barkof, Frederick, Muller, Majon, Breteler, Monique MB, Román, Gustavo C, Hamel, Edith, Seshadri, Sudha, Gottesman, Rebecca F, van Buchem, Mark A, Arvanitakis, Zoe, Schneider, Julie A, Drewes, Lester R, Hachinski, Vladimir, Finch, Caleb E, Toga, Arthur W, Wardlaw, Joanna M, and Zlokovic, Berislav V

Subjects
Blood-Brain Barrier, Brain, Humans, Alzheimer Disease, Vascular Diseases, Cerebrovascular Circulation, United States, National Institute on Aging (U.S.), Amyloid beta-Peptides, White Matter, Biomarkers, Alzheimer's disease, Blood-brain barrier, Cerebral blood flow, MRI, Vascular, National Institute on Aging, Neurosciences, Clinical Sciences, Geriatrics
Abstract

Increasing evidence recognizes Alzheimer's disease (AD) as a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including vascular dysfunction. The recently updated AD Research Framework put forth by the National Institute on Aging-Alzheimer's Association describes a biomarker-based pathologic definition of AD focused on amyloid, tau, and neuronal injury. In response to this article, here we first discussed evidence that vascular dysfunction is an important early event in AD pathophysiology. Next, we examined various imaging sequences that could be easily implemented to evaluate different types of vascular dysfunction associated with, and/or contributing to, AD pathophysiology, including changes in blood-brain barrier integrity and cerebral blood flow. Vascular imaging biomarkers of small vessel disease of the brain, which is responsible for >50% of dementia worldwide, including AD, are already established, well characterized, and easy to recognize. We suggest that these vascular biomarkers should be incorporated into the AD Research Framework to gain a better understanding of AD pathophysiology and aid in treatment efforts.

Published
2019

40. The glymphatic system: Current understanding and modeling

Author

Bohr, Tomas, Hjorth, Poul G., Holst, Sebastian C., Hrabětová, Sabina, Kiviniemi, Vesa, Lilius, Tuomas, Lundgaard, Iben, Mardal, Kent-Andre, Martens, Erik A., Mori, Yuki, Nägerl, U. Valentin, Nicholson, Charles, Tannenbaum, Allen, Thomas, John H., Tithof, Jeffrey, Benveniste, Helene, Iliff, Jeffrey J., Kelley, Douglas H., and Nedergaard, Maiken

Published
2022
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46. The Alzheimer's disease 5xFAD mouse model is best suited to investigate pretargeted imaging approaches beyond the blood-brain barrier.

Author

Lopes van den Broek, Sara, Sehlin, Dag, Andersen, Jens V., Aldana, Blanca I., Beschörner, Natalie, Nedergaard, Maiken, Knudsen, Gitte M., Syvänen, Stina, and Herth, Matthias M.

Subjects
ALZHEIMER'S disease diagnosis, BIOLOGICAL models, TRANSGENIC animals, RESEARCH funding, BLOOD-brain barrier, IMMUNOGLOBULINS, BRAIN, POSITRON emission tomography, LIGATURE (Surgery), IN vivo studies, MICE, ANIMAL experimentation, EARLY diagnosis, COMPARATIVE studies, GENETIC mutation, CEREBELLUM, AMYLOID beta-protein precursor, CONTRAST media
Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease, with an increasing prevalence. Currently, there is no ideal diagnostic molecular imaging agent for diagnosing AD. Antibodies (Abs) have been proposed to close this gap as they can bind selectively and with high affinity to amyloid β (Aβ)--one of the molecular hallmarks of AD. Abs can even be designed to selectively bind Aβ oligomers or isoforms, which are difficult to target with small imaging agents. Conventionally, Abs must be labeled with long-lived radionuclides which typically results in in high radiation burden to healthy tissue. Pretargeted imaging could solve this challenge as it allows for the use of short-lived radionuclides. To develop pretargeted imaging tools that can enter the brain, AD mouse models are useful as they allow testing of the imaging approach in a relevant animal model that could predict its clinical applicability. Several mouse models for AD have been developed with different characteristics. Commonly used models are: 5xFAD, APP/PS1 and tg-ArcSwe transgenic mice. In this study, we aimed to identify which of these models were best suited to investigate pretargeted imaging approaches beyond the blood brain barrier. We evaluated this by pretargeted autoradiography using the Aβ-targeting antibody 3D6 and an 111In-labeled Tz. Evaluation criteria were target-to-background ratios and accessibility. APP/PS1 mice showed Aβ accumulation in high and low binding brain regions and is as such less suitable for pretargeted purposes. 5xFAD and tg-ArcSwe mice showed similar uptake in high binding regions whereas low uptake in low binding regions and are better suited to evaluate pretargeted imaging approaches. 5xFAD mice are advantaged over tg-ArcSwe mice as pathology can be traced early (6 months compared to 18 months of age) and as 5xFAD mice are commercially available. [ABSTRACT FROM AUTHOR]

Published
2024
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47. Human brain clearance imaging: Pathways taken by magnetic resonance imaging contrast agents after administration in cerebrospinal fluid and blood.

Author

van Osch, Matthias J. P., Wåhlin, Anders, Scheyhing, Paul, Mossige, Ingrid, Hirschler, Lydiane, Eklund, Anders, Mogensen, Klara, Gomolka, Ryszard, Radbruch, Alexander, Qvarlander, Sara, Decker, Andreas, Nedergaard, Maiken, Mori, Yuki, Eide, Per Kristian, Deike, Katerina, and Ringstad, Geir

Subjects
MAGNETIC resonance imaging, INTRAVENOUS injections, INTRATHECAL injections, CONTRAST media, CEREBROSPINAL fluid
Abstract

Over the last decade, it has become evident that cerebrospinal fluid (CSF) plays a pivotal role in brain solute clearance through perivascular pathways and interactions between the brain and meningeal lymphatic vessels. Whereas most of this fundamental knowledge was gained from rodent models, human brain clearance imaging has provided important insights into the human system and highlighted the existence of important interspecies differences. Current gold standard techniques for human brain clearance imaging involve the injection of gadolinium‐based contrast agents and monitoring their distribution and clearance over a period from a few hours up to 2 days. With both intrathecal and intravenous injections being used, which each have their own specific routes of distribution and thus clearance of contrast agent, a clear understanding of the kinetics associated with both approaches, and especially the differences between them, is needed to properly interpret the results. Because it is known that intrathecally injected contrast agent reaches the blood, albeit in small concentrations, and that similarly some of the intravenously injected agent can be detected in CSF, both pathways are connected and will, in theory, reach the same compartments. However, because of clear differences in relative enhancement patterns, both injection approaches will result in varying sensitivities for assessment of different subparts of the brain clearance system. In this opinion review article, the "EU Joint Programme – Neurodegenerative Disease Research (JPND)" consortium on human brain clearance imaging provides an overview of contrast agent pharmacokinetics in vivo following intrathecal and intravenous injections and what typical concentrations and concentration–time curves should be expected. This can be the basis for optimizing and interpreting contrast‐enhanced MRI for brain clearance imaging. Furthermore, this can shed light on how molecules may exchange between blood, brain, and CSF. [ABSTRACT FROM AUTHOR]

Published
2024
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48. Chronic sleep fragmentation impairs brain interstitial clearance in young wildtype mice.

Author

Deng, Saiyue, Hu, Yusi, Chen, Simiao, Xue, Yang, Yao, Di, Sun, Qian, Nedergaard, Maiken, Wang, Wei, and Ding, Fengfei

Abstract

Accumulating evidence shows that most chronic neurological diseases have a link with sleep disturbances, and that patients with chronically poor sleep undergo an accelerated cognitive decline. Indeed, a single-night of sleep deprivation may increase metabolic waste levels in cerebrospinal fluid. However, it remains unknown how chronic sleep disturbances in isolation from an underlying neurological disease may affect the glymphatic system. Clearance of brain interstitial waste by the glymphatic system occurs primarily during sleep, driven by multiple oscillators including arterial pulsatility, and vasomotion. Herein, we induced sleep fragmentation in young wildtype mice and assessed the effects on glymphatic activity and cognitive functions. Chronic sleep fragmentation reduced glymphatic function and impaired cognitive functions in healthy mice. A mechanistic analysis showed that the chronic sleep fragmentation suppressed slow vasomotion, without altering cardiac-driven pulsations. Taken together, results of this study document that chronic sleep fragmentation suppresses brain metabolite clearance and impairs cognition, even in the absence of disease. [ABSTRACT FROM AUTHOR]

Published
2024
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