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1,044 results on '"Nedergaard, Maiken"'

10. 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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28. 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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34. 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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35. 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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39. The Ocular Glymphatic System—Current Understanding and Future Perspectives.

Author

Delle, Christine, Wang, Xiaowei, and Nedergaard, Maiken

Subjects
MACULAR degeneration, AXONAL transport, DIABETIC retinopathy, CEREBROSPINAL fluid, OPTIC nerve, RETINA
Abstract

The ocular glymphatic system subserves the bidirectional polarized fluid transport in the optic nerve, whereby cerebrospinal fluid from the brain is directed along periarterial spaces towards the eye, and fluid from the retina is directed along perivenous spaces following upon its axonal transport across the glial lamina. Fluid homeostasis and waste removal are vital for retinal function, making the ocular glymphatic fluid pathway a potential route for targeted manipulation to combat blinding ocular diseases such as age-related macular degeneration, diabetic retinopathy, and glaucoma. Several lines of work investigating the bidirectional ocular glymphatic transport with varying methodologies have developed diverging mechanistic models, which has created some confusion about how ocular glymphatic transport should be defined. In this review, we provide a comprehensive summary of the current understanding of the ocular glymphatic system, aiming to address misconceptions and foster a cohesive understanding of the topic. [ABSTRACT FROM AUTHOR]

Published
2024
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40. Dysregulation of extracellular potassium distinguishes healthy ageing from neurodegeneration.

Author

Ding, Fengfei, Sun, Qian, Long, Carter, Rasmussen, Rune Nguyen, Peng, Sisi, Xu, Qiwu, Kang, Ning, Song, Wei, Weikop, Pia, Goldman, Steven A, and Nedergaard, Maiken

Subjects
HUNTINGTON disease, ALZHEIMER'S disease, AMYOTROPHIC lateral sclerosis, NEURODEGENERATION, POTASSIUM channels
Abstract

Progressive neuronal loss is a hallmark feature distinguishing neurodegenerative diseases from normal ageing. However, the underlying mechanisms remain unknown. Extracellular K+ homeostasis is a potential mediator of neuronal injury as K+ elevations increase excitatory activity. The dysregulation of extracellular K+ and potassium channel expressions during neurodegeneration could contribute to this distinction. Here we measured the cortical extracellular K+ concentration ([K+]e) in awake wild-type mice as well as murine models of neurodegeneration using K+-sensitive microelectrodes. Unexpectedly, aged wild-type mice exhibited significantly lower cortical [K+]e than young mice. In contrast, cortical [K+]e was consistently elevated in Alzheimer's disease (APP/PS1), amyotrophic lateral sclerosis (ALS) (SOD1G93A) and Huntington's disease (R6/2) models. Cortical resting [K+]e correlated inversely with neuronal density and the [K+]e buffering rate but correlated positively with the predicted neuronal firing rate. Screening of astrocyte-selective genomic datasets revealed a number of potassium channel genes that were downregulated in these disease models but not in normal ageing. In particular, the inwardly rectifying potassium channel Kcnj10 was downregulated in ALS and Huntington's disease models but not in normal ageing, while Fxyd1 and Slc1a3 , each of which acts as a negative regulator of potassium uptake, were each upregulated by astrocytes in both Alzheimer's disease and ALS models. Chronic elevation of [K+]e in response to changes in gene expression and the attendant neuronal hyperexcitability may drive the neuronal loss characteristic of these neurodegenerative diseases. These observations suggest that the dysregulation of extracellular K+ homeostasis in a number of neurodegenerative diseases could be due to aberrant astrocytic K+ buffering and as such, highlight a fundamental role for glial dysfunction in neurodegeneration. [ABSTRACT FROM AUTHOR]

Published
2024
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44. 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 P. J., 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

Published
2020
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