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pro vyhledávání: '"somatodendritic compartment"'
Akademický článek
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Autor:
Ines Noher, Mariano Bisbal, Ana Clara Venier, Favio Pesaola, Ana Lucía De Paul, Gonzalo Quassollo
Publikováno v:
Biology of the Cell. 113:419-437
Background information The endo-lysosomal system (ELS) comprises a set of membranous organelles responsible for transporting intracellular and extracellular components within cells. Defects in lysosomal proteins usually affect a large variety of proc
Autor:
Jaerin Sohn, Shinichiro Okamoto, Naoya Kataoka, Takeshi Kaneko, Kazuhiro Nakamura, Hiroyuki Hioki
Publikováno v:
Frontiers in Neuroanatomy, Vol 10 (2016)
The recurrent network composed of excitatory and inhibitory neurons is fundamental to neocortical function. Inhibitory neurons in the mammalian neocortex are molecularly diverse, and individual cell types play unique functional roles in the neocortic
Externí odkaz:
https://doaj.org/article/e3e19bb177e9434694d149e14b0ab2f6
Autor:
Patrik Verstreken, Dietmar Rudolf Thal, Rik Vandenberghe, Thomas Tousseyn, Luis Aragão Gomes, Christine A. F. von Arnim, Diego Lopez-Sanmartin, Sandra O. Tomé, Mathieu Vandenbulcke, Valerie Uytterhoeven
Publikováno v:
Acta Neuropathologica
In Alzheimer's disease (AD), tau-protein undergoes a multi-step process involving the transition from a natively unfolded monomer to large, aggregated structures such as neurofibrillary tangles (NFTs). However, it is not yet clear which events initia
INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury
Autor:
Tatyana Svitkina, Uri Manor, Henry N. Higgs, Jones S, Lingelbach Mj, Barbara Calabrese, Shelley Halpain, Andy Y. Shih, Yamaguchi-Shiraishi Y
During early stages of ischemic brain injury, glutamate receptor hyperactivation mediates neuronal death via osmotic cell swelling. Here we show that ischemia and excess NMDA receptor activation – conditions that trigger neuronal swelling -- cause
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::97ac480ee036f10cd40a0907f75dc5e9
https://doi.org/10.1101/2021.10.01.462790
https://doi.org/10.1101/2021.10.01.462790
Publikováno v:
Frontiers in Molecular Neuroscience, Vol 14 (2021)
Frontiers in Molecular Neuroscience
Frontiers in Molecular Neuroscience
Microtubule-associated protein tau forms insoluble neurofibrillary tangles (NFTs), which is one of the major histopathological hallmarks of Alzheimer’s disease (AD). Many studies have demonstrated that tau causes early functional deficits prior to
Autor:
Peijie Chen, Binglin Chen, Yi Zhu, Meng-Si Peng, Xue-Qiang Wang, Yi-Li Zheng, Jing‐Zhao Yang, Hao-Yu Hu, Chang-Cheng Chen, Ge Song, Jia-Bao Guo
Publikováno v:
Journal of Cellular and Molecular Medicine
The molecular mechanisms underlying neuropathic pain (NP) remain poorly understood. Emerging evidence has suggested the role of microRNAs (miRNAs) in the initiation and development of NP, but the specific effects of miRNAs in NP are largely unknown.
Publikováno v:
Acta Neuropathologica Communications, Vol 7, Iss 1, Pp 1-21 (2019)
Acta Neuropathologica Communications
Acta Neuropathologica Communications
The deposition of tau pathology in Alzheimer’s disease (AD) may occur first in axons of neurons and then progress back into the cell bodies to form neurofibrillary tangles, however, studies have not directly analyzed this relationship in relatively
Autor:
Satoko Wada-Kakuda, Akane Nomori, Makoto Matsuyama, Tomohiro Miyasaka, Yasuo Ihara, Mitsuhiro Kawata, Shigeo Murayama, Atsuko Kubo, Akihiko Takashima, Hiroaki Misonou
Publikováno v:
The Journal of Comparative Neurology
Abtract Tau is a microtubule‐associated protein (MAP) that is localized to the axon. In Alzheimer's disease (AD), the distribution of tau undergoes a remarkable alteration, leading to the formation of tau inclusions in the somatodendritic compartme
Autor:
Emmanuel Brouillet, Julien Flament, Jean-Baptiste Perot, Kalina Wiatr, Maciej Figiel, L. Marczak
Publikováno v:
Frontiers in Molecular Neuroscience
Frontiers in Molecular Neuroscience, Vol 14 (2021)
Frontiers in Molecular Neuroscience, Vol 14 (2021)
Spinocerebellar ataxia type 3 (SCA3/MJD) is caused by CAG expansion mutation resulting in a long polyQ domain in mutant ataxin-3. The mutant protein is a special type of protease, deubiquitinase, which may indicate its prominent impact on the regulat