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65,677 results on '"neuron"'

28. Rapid iPSC inclusionopathy models shed light on formation, consequence, and molecular subtype of α-synuclein inclusions

Author

Lam, Isabel, Ndayisaba, Alain, Lewis, Amanda J., Fu, YuHong, Sagredo, Giselle T., Kuzkina, Anastasia, Zaccagnini, Ludovica, Celikag, Meral, Sandoe, Jackson, Sanz, Ricardo L., Vahdatshoar, Aazam, Martin, Timothy D., Morshed, Nader, Ichihashi, Toru, Tripathi, Arati, Ramalingam, Nagendran, Oettgen-Suazo, Charlotte, Bartels, Theresa, Boussouf, Manel, Schäbinger, Max, Hallacli, Erinc, Jiang, Xin, Verma, Amrita, Tea, Challana, Wang, Zichen, Hakozaki, Hiroyuki, Yu, Xiao, Hyles, Kelly, Park, Chansaem, Wang, Xinyuan, Theunissen, Thorold W., Wang, Haoyi, Jaenisch, Rudolf, Lindquist, Susan, Stevens, Beth, Stefanova, Nadia, Wenning, Gregor, van de Berg, Wilma D.J., Luk, Kelvin C., Sanchez-Pernaute, Rosario, Gómez-Esteban, Juan Carlos, Felsky, Daniel, Kiyota, Yasujiro, Sahni, Nidhi, Yi, S. Stephen, Chung, Chee Yeun, Stahlberg, Henning, Ferrer, Isidro, Schöneberg, Johannes, Elledge, Stephen J., Dettmer, Ulf, Halliday, Glenda M., Bartels, Tim, and Khurana, Vikram

Published
2024
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46. Current-Sensing ADC with Power Consumption of 57 nW and FoM of 336 fJ/Conversion at 28 nm CMOS Technology

Author

Singhal, Navin, Santosh, M., Bose, S. C., Karmakar, Abhijit, Angrisani, Leopoldo, Series Editor, Arteaga, Marco, Series Editor, Chakraborty, Samarjit, Series Editor, Chen, Shanben, Series Editor, Chen, Tan Kay, Series Editor, Dillmann, Rüdiger, Series Editor, Duan, Haibin, Series Editor, Ferrari, Gianluigi, Series Editor, Ferre, Manuel, Series Editor, Hirche, Sandra, Series Editor, Jabbari, Faryar, Series Editor, Jia, Limin, Series Editor, Kacprzyk, Janusz, Series Editor, Khamis, Alaa, Series Editor, Kroeger, Torsten, Series Editor, Li, Yong, Series Editor, Liang, Qilian, Series Editor, Martín, Ferran, Series Editor, Ming, Tan Cher, Series Editor, Minker, Wolfgang, Series Editor, Misra, Pradeep, Series Editor, Mukhopadhyay, Subhas, Series Editor, Ning, Cun-Zheng, Series Editor, Nishida, Toyoaki, Series Editor, Oneto, Luca, Series Editor, Panigrahi, Bijaya Ketan, Series Editor, Pascucci, Federica, Series Editor, Qin, Yong, Series Editor, Seng, Gan Woon, Series Editor, Speidel, Joachim, Series Editor, Veiga, Germano, Series Editor, Wu, Haitao, Series Editor, Zamboni, Walter, Series Editor, Tan, Kay Chen, Series Editor, Gupta, Anu, editor, Pandey, Jai Gopal, editor, Chaturvedi, Nitin, editor, and Dwivedi, Devesh, editor

Published
2025
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50. Cofilactin rod formation mediates inflammation-induced neurite degeneration

Author

Uruk, Gökhan, Mocanu, Ebony, Shaw, Alisa E, Bamburg, James R, and Swanson, Raymond A

Subjects
Biochemistry and Cell Biology, Biological Sciences, Neurosciences, Neurodegenerative, Aetiology, 2.1 Biological and endogenous factors, Neurological, CP: Neuroscience, NADPH-oxidase, actin, axon, cofilin-1, dendrite, inflammation, microglia, neuron, superoxide, Medical Physiology, Biological sciences
Abstract

Stroke, trauma, and neurodegenerative disorders cause loss of neurites (axons and dendrites) in addition to neuronal death. Neurite loss may result directly from a primary insult, secondary to parental neuron death, or secondary to a post-injury inflammatory response. Here, we use lipopolysaccharide and the alarmin S100β to selectively evaluate neurite loss caused by the inflammatory response. Activation of microglia and infiltrating macrophages by these stimuli causes neurite loss that far exceeds neuronal death, both in vitro and in vivo. Neurite loss is accompanied by the formation of cofilactin rods and aggregates (CARs), which are polymers of cofilin-1 and actin induced by oxidative stress and other factors. Mice deficient in either cofilin-1 or the superoxide-generating enzyme NADPH oxidase-2 show reduced CAR formation, neurite loss, and motor impairment. The findings identify a mechanism by which inflammation leads to neurite loss via CAR formation and highlight the relevance of neurite loss to functional impairment.

Published
2024

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