The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis
Open accessAbstract
Dominant mutations in superoxide dismutase cause amyotrophic lateral sclerosis (ALS), an adult-onset neurodegenerative disease that is characterized by the loss of motor neurons. Using mice carrying a deletable mutant gene, diminished mutant expression in astrocytes did not affect onset, but delayed microglial activation and sharply slowed later disease progression. These findings demonstrate that mutant astrocytes are viable targets for therapies for slowing the progression of non-cell autonomous killing of motor neurons in ALS.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Selectively deleting mutant SOD1 transgene expression in astrocytes, sharply slows the disease progression in the SOD1 mouse model of ALS [22].”
From Distinct repertoires of microRNAs present in mouse astrocytes compared to astrocyte-secreted exosomes (2017) · cites this paper as [22]
In the citing paper
“In pre-symptomatic mutant SOD1 transgenic mice, activated microglia initially display neuroprotective properties that slow disease progression;”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [436]
In the citing paper
“however, with time the continued and unabridged neuroinflammation only enhances neurodegeneration and accelerates disease progression [434–436].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [436]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Onset and Progression in Inherited ALS Determined by Motor Neurons and Microglia
Boillée, S., Yamanaka, K., Lobsiger, C. S., Copeland, N. G., Jenkins, N. A., Kassiotis, G., Kollias, G., & Cleveland, D. W. (2006) · Science · doi:10.1126/science.1123511 · Cited by 1,623
Self-citationALS: A Disease of Motor Neurons and Their Nonneuronal Neighbors
Boillée, S., Velde, C. V., & Cleveland, D. W. (2006) · Neuron · doi:10.1016/j.neuron.2006.09.018 · Cited by 1,476
Self-citationAstrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons
Nagai, M., Re, D. B., Nagata, T., Chalazonitis, A., Jessell, T. M., Wichterle, H., & Przedborski, S. (2007) · Nature Neuroscience · doi:10.1038/nn1876 · Cited by 1,220
Wild-Type Nonneuronal Cells Extend Survival of SOD1 Mutant Motor Neurons in ALS Mice
Clement, A. M., Nguyen, M. D., Roberts, E. A., Garcia, M. L., Boillée, S., Rule, M., McMahon, A. P., Doucette, W. T., Siwek, D. F., Ferrante, R. J., et al. (2003) · Science · doi:10.1126/science.1086071 · Cited by 1,131
Self-citationMolecular biology of amyotrophic lateral sclerosis: insights from genetics
Pasinelli, P., & Brown, R. H. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1971 · Cited by 1,107
Howland, D., Liu, J., She, Y., Goad, B., Maragakis, N. J., Kim, B. B., Erickson, J., Kulik, J., DeVito, L., Psaltis, G. C., et al. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.032539299 · Cited by 890
Self-citationNon–cell autonomous effect of glia on motor neurons in an embryonic stem cell–based ALS model
Di Giorgio, F. P., Carrasco, M. A., Siao, M. C., Maniatis, T., & Eggan, K. (2007) · Nature Neuroscience · doi:10.1038/nn1885 · Cited by 799
Beers, D. R., Henkel, J. S., Xiao, Q., Zhao, W., Wang, J., Yen, A. A., Siklos, L., McKercher, S. R., & Appel, S. H. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0607423103 · Cited by 733
A role for astrocytes in motor neuron loss in amyotrophic lateral sclerosis
Barbeito, L., Pehar, M., Cassina, P., Vargas, M. R., Peluffo, H., Viera, L., Estévez, Á. G., & Beckman, J. S. (2004) · Brain Research Reviews · doi:10.1016/j.brainresrev.2004.05.003 · Cited by 331
Bajenaru, M. L., Zhu, Y., Hedrick, N. M., Donahoe, J. S., Parada, L. F., & Gutmann, D. H. (2002) · Molecular and Cellular Biology · doi:10.1128/mcb.22.14.5100-5113.2002 · Cited by 322
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Items 801–900 of 1,000
Targeting mitochondrial Ca2+ uptake for the treatment of amyotrophic lateral sclerosis
Zhong, R., Rua, M. T., & Wei‐LaPierre, L. (2023) · The Journal of Physiology · doi:10.1113/jp284143 · Cited by 12
“…in ALS pathology for decades (gliosis), particularly the involvement of astrocytes and microglia (Boillée et al., 2006; Filipi et al., 2020; Gerber et al., 2012; Lasiene & Yamanaka, 2011; Murphy-Royal et al., 2017; Philips & Rothstein, 2014; Verkhratsky & Semyanov, 2022; Yamanaka et al., 2008).”
BackgroundMartínez, P., Silva, M., Abarzúa, S., Tevy, M. F., Jaimovich, E., Constantine‐Paton, M., Bustos, F. J., & van Zundert, B. (2024) · Molecular Medicine · doi:10.1186/s10020-024-00942-4 · Cited by 13
Wang, Y., & Patani, R. (2020) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2020.1805734 · Cited by 10
“specific expression of mutant superoxide dismutase 1 (SOD1) [9,10].”
BackgroundClioquinol kills astrocyte-derived KT-5 cells by the impairment of the autophagy–lysosome pathway
Mizutani, Y., Maeda, T., Murate, K., Ito, S., Watanabe, H., & Mutoh, T. (2020) · Archives of Toxicology · doi:10.1007/s00204-020-02943-8 · Cited by 10
Torazza, C., Provenzano, F., Gallia, E., Cerminara, M., Balbi, M., Bonifacino, T., Tessitore, S., Ravera, S., Usai, C., Musante, I., et al. (2023) · Cells · doi:10.3390/cells12151952 · Cited by 11
“Astrocytes can affect MNs by transferring reactive oxygen/nitrogen species, complement components, chemokines, and cytokines [25,26]; modulating the microglial inflammatory response [27]; and reducing the efflux of lactate from oligodendrocytes for MN energy demand [24], all concurring to the development of Glu-mediat…”
BackgroundLemos, J. P., Tenório, L. P. G., Mouly, V., Butler-Browne, G. S., Mendes‐da‐Cruz, D. A., Savino, W., & Smeriglio, P. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1202834 · Cited by 10
“Similarly, selective reduction of mSOD1 in microglia or astrocytes of ALS mice increases their survival (73, 74).”
BackgroundAlves, C. J., Maximino, J. R., & Chadi, G. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00332 · Cited by 12
Astrocyte–Neuron Communications
McIver, S. R., Faideau, M., & Haydon, P. G. (2012) · Springer eBooks · doi:10.1007/978-1-4614-4729-0_2 · Cited by 12
“When mutant SOD1 is absent in astrocytes only, astrogliosis, but not microgliosis, is delayed compared to mice with ubiquitous expression of mutant SOD1 [ 225 ] .”
BackgroundInfluentialOhta, Y., Nagai, M., Miyazaki, K., Tanaka, N., Kawai, H., Mimoto, T., Morimoto, N., Kurata, T., Ikeda, Y., Matsuura, T., et al. (2011) · Cell Medicine · doi:10.3727/215517910x582779 · Cited by 10
Kaur, K. K., Allahbadia, G. N., & Singh, M. (2017) · Obesity Research - Open Journal · doi:10.17140/oroj-4-132 · Cited by 9
SOD1/Rag2 Mice with Low Copy Number of SOD1 Gene as a New Long-Living Immunodeficient Model of ALS
Majchrzak, M., Drela, K., Andrzejewska, A., Rogujski, P., Figurska, S., Fiedorowicz, M., Walczak, P., Janowski, M., Łukomska, B., & Stanaszek, L. (2019) · Scientific Reports · doi:10.1038/s41598-018-37235-w · Cited by 10
NMR-Guided Design of Potent and Selective EphA4 Agonistic Ligands
Baggio, C., Kulinich, A. O., Dennys, C. N., Rodrigo, R., Meyer, K., Ethell, I. M., & Pellecchia, M. (2021) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.1c00608 · Cited by 10
Perić, M., Nikolic, L. M., Anđjus, P. R., & Bataveljić, D. (2021) · European Journal of Neuroscience · doi:10.1111/ejn.15451 · Cited by 11
“The expression of mutant SOD1 in non-neuronal cells showed to be harmful to motor neurons and to accelerate the disease progression (Boillee et al., 2006; Yamanaka et al., 2008).”
BackgroundMalada-Edelstein, Y. F., Solomonov, Y., Hadad, N., Alfahel, L., Israelson, A., & Lévy, R. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02326-5 · Cited by 10
Why do motor neurons degenerate? Actualisation in the pathogenesis of amyotrophic lateral sclerosis
Riancho, J., Gonzalo, I., Ruiz‐Soto, M., & Berciano, J. (2017) · Neurología (English Edition) · doi:10.1016/j.nrleng.2015.12.019 · Cited by 11
Parpura, V., & Verkhratsky, A. (2012) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2012.11.023 · Cited by 11
Murakami, G., Inoue, H., Tsukita, K., Asai, Y., Amagai, Y., Aiba, K., Shimogawa, H., Uesugi, M., Nakatsuji, N., & Takahashi, R. (2011) · SLAS DISCOVERY · doi:10.1177/1087057110397888 · Cited by 10
Self-citationMitsui, S., Otomo, A., Sato, K., Ishiyama, M., Shimakura, K., Okada-Yamaguchi, C., Warabi, E., Yanagawa, T., Aoki, M., Shang, H., et al. (2022) · Neurochemistry International · doi:10.1016/j.neuint.2022.105364 · Cited by 8
Adachi, K., Miyata, K., Chida, Y., Hirose, M., Morisaki, Y., Yamanaka, K., & Misawa, H. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1291673 · Cited by 9
Self-citationIyer, A. K., Schoch, K. M., Verbeck, A. C., Galasso, G., Chen, H., Smith, S. E., Oldenborg, A., Miller, T. M., Karch, C. M. M., & Bonni, A. (2023) · PLoS ONE · doi:10.1371/journal.pone.0294731 · Cited by 9
Towards an integrated approach for understanding glia in Amyotrophic Lateral Sclerosis
Majewski, S., Klein, P., Boillée, S., Clarke, B. E., & Patani, R. (2024) · Glia · doi:10.1002/glia.24622 · Cited by 8
Role of Mitochondrial Dysfunction in Motor Neuron Degeneration in ALS
Diana, L. G., Ramírez-Jarquín, U. N., & Tapi, R. (2012) · InTech eBooks · doi:10.5772/31290 · Cited by 9
“4 Inflammation A mechanism of non-cell-autonomous death associated with motor neuron degeneration in both FALS and SALS is the participation of non-neuronal cells in inflammatory events (Boillee et al., 2006a; Boillee et al., 2006b; Hall et al., 1998; Yamanaka et al., 2008; Yang et al., 2011).”
BackgroundMicroglia in neurodegenerative disorders and neuroinflammation
Suzumura, A. (2014) · Rinsho Shinkeigaku · doi:10.5692/clinicalneurol.54.1119 · Cited by 9
Free fatty acids support oligodendrocyte survival in a mouse model of amyotrophic lateral sclerosis
Maruyama, T., Tanabe, S., Uyeda, A., Suzuki, T., & Muramatsu, R. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1081190 · Cited by 9
“Emerging evidence has suggested that ALS is not merely a disease of MNs, and that their interactions with glial cells, including astrocytes, microglia, and oligodendrocytes (OLs), also mediate the pathology of ALS (Boillée et al., 2006; Yamanaka et al., 2008; Puentes et al., 2016).”
BackgroundVerkhratsky, A., & Butt, A. M. (2023) · Elsevier eBooks · doi:10.1016/b978-0-12-821565-4.00012-2 · Cited by 10
Nanclares, C., Noriega‐Prieto, J. A., Labrada-Moncada, F. E., Cvetanović, M., Araque, A., & Kofuji, P. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106318 · Cited by 12
“…Jiang et al., 2016; Meunier et al., 2016), Parkinson ’ s disease (Halliday and Stevens, 2011; Díaz et al., 2019), amyotrophic lateral sclerosis (Yamanaka et al., 2008), and some forms of ataxia (Kretzschmar et al., 2005; Custer et al., 2006; Furrer et al., 2011), including SCA1 (Kim et al.,…”
Aberrant CHCHD2-associated mitochondriopathy in Kii ALS/PDC astrocytes
Leventoux, N., Morimoto, S., Ishikawa, M., Nakamura, S., Ozawa, F., Kobayashi, R., Watanabe, H., Supakul, S., Okamoto, S., Zhou, Z., et al. (2024) · Acta Neuropathologica · doi:10.1007/s00401-024-02734-w · Cited by 10
“The contribution of astrocytes to the progression of ALS has been reported [31, 32, 100, 162].”
Self-citationOxidative stress sensitivity in ALS muscle cells
Dupuis, L. (2009) · Experimental Neurology · doi:10.1016/j.expneurol.2009.08.023 · Cited by 9
“Recent work however challenged this “neurocentric” view by showing that other cell types, notably glial cells and myofibers, participate in the triggering of motor neuron degeneration (Boillee et al., 2006a,b, Clement et al., 2003; Dobrowolny et al., 2008; Yamanaka et al., 2008).”
Up-regulated inflammatory signatures of the spinal cord in canine degenerative myelopathy
Hashimoto, K., Kobatake, Y., Asahina, R., Yamato, O., Islam, M. S., Sakai, H., Nishida, H., Maeda, S., & Kamishina, H. (2020) · Research in Veterinary Science · doi:10.1016/j.rvsc.2020.11.001 · Cited by 10
Sekiya, M., Ichiyanagi, T., Ikeshiro, Y., & Yokozawa, T. (2009) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.32.382 · Cited by 9
Reappraisal of VAChT‐Cre: Preference in slow motor neurons innervating type I or IIa muscle fibers
Misawa, H., Inomata, D., Kikuchi, M., Maruyama, S., Moriwaki, Y., Okuda, T., Nukina, N., & Yamanaka, T. (2016) · genesis · doi:10.1002/dvg.22979 · Cited by 9
“The VAChTCre lines have been used in various research settings for introducing MN-specific gene modifications (Haramanti et al., 2010; Hideyama et al., 2010; Iguchi et al., 2013; Lecomte et al., 2014; Misawa et al., 2006; Tashiro et al., 2012; Yamanaka et al., 2008; Zhai et al., 2011).”
MethodSelf-citationCord blood as a potential therapeutic for amyotrophic lateral sclerosis
Garbuzova-Davis, S. N., Ehrhart, J. C., & Sanberg, P. R. (2017) · Expert Opinion on Biological Therapy · doi:10.1080/14712598.2017.1323862 · Cited by 9
Thonhoff, J. R., Gao, J., Dunn, T. J., Ojeda, L. D., & Wu, P. (2012) · Europe PMC (PubMed Central) · Cited by 9
Yamamoto, M., Tanaka, F., Tatsumi, H., & Sobue, G. (2008) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.9.11.1845 · Cited by 9
Lee, J. H., Chang, W. S., Min, S. S., Song, D., & Yoo, H. (2025) · Cells · doi:10.3390/cells14171342 · Cited by 8
Neuroprotective effects of violacein in a model of inherited amyotrophic lateral sclerosis
Olivera‐Bravo, S., Bolatto, C., Damianovich, G. O., Stancov, M., Cerri, S., Rodríguez, P., Boragno, D., Mir, K. H., Cuitiño, M. N., Larrambembere, F., et al. (2022) · Scientific Reports · doi:10.1038/s41598-022-06470-7 · Cited by 9
“3), the number of hydrogen bond donors (4) together with the sum of all nitrogens and oxygens (6) indicates that violacein ́s molecular structure fulfills the thresholds of the Lipinski’s rules for molecules able to cross the BBB39.”
BackgroundSulforaphane Upregulates Cultured Mouse Astrocytic Aquaporin-4 Expression through p38 MAPK Pathway
Yang, C., Qin, S., Zhang, J., Wang, Y., Li, H., & Lü, T. (2022) · Journal of Healthcare Engineering · doi:10.1155/2022/1144124 · Cited by 8
Regulation of Microglial Signaling by Lyn and SHIP-1 in the Steady-State Adult Mouse Brain
Chu, E., Mychasiuk, R., Tsantikos, E., Raftery, A. L., L’Estrange-Stranieri, E., Dill, L. K., Semple, B. D., & Hibbs, M. L. (2023) · Cells · doi:10.3390/cells12192378 · Cited by 8
“As such, dysregulated neuroimmune responses have been increasingly implicated in various neurodegenerative diseases and psychological disorders [3,4].”
BackgroundGlial evolution as a determinant of human behavior and its disorders
Goldman, S. A. (2020) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.14372 · Cited by 9
Bicchi, I., Morena, F., Argentati, C., Nodari, L. R., Emiliani, C., Gelati, M., Vescovi, A. L., & Martino, S. (2021) · Biomedicines · doi:10.3390/biomedicines9091080 · Cited by 8
Amyotrophic lateral sclerosis: applications of stem cells – an update
Cova, L., & Silani, V. (2010) · Stem Cells and Cloning Advances and Applications · doi:10.2147/sccaa.s8662 · Cited by 8
Milosevic, M. M., Bataveljić, D., Nikolic, L. M., Bijelić, D. D., & Anđjus, P. R. (2016) · Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration · doi:10.3109/21678421.2016.1143516 · Cited by 8
“The importance of cell-cell interaction between motor neurons and their non-neuronal neighbours (astrocytes and microglia) has been implicated in the rate of disease progression in ALS (7,8).”
BackgroundModelling FUS Mislocalisation in an In Vitro Model of Innervated Human Muscle
Mihevc, S. P., Pavlin, M., Darovic, S., Živin, M., Podbregar, M., Rogelj, B., & Marš, T. (2017) · Journal of Molecular Neuroscience · doi:10.1007/s12031-017-0940-y · Cited by 8
Ji, Y., Duan, W., Liu, Y., Liu, Y., Liu, C., Li, Y., Wen, D., Li, Z., & Li, C. (2017) · Neuroscience Letters · doi:10.1016/j.neulet.2017.12.062 · Cited by 8
Single-cell transcriptomic analysis of the adult mouse spinal cordPreprint
Blum, J. A., Klemm, S. L., Nakayama, L., Kathiria, A. S., Guttenplan, K. A., Hoang, P. T., Shadrach, J. L., Kaltschmidt, J. A., Greenleaf, W. J., & Gitler, A. D. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.03.16.992958 · Cited by 8
TNFα prevents FGF4-mediated rescue of astrocyte dysfunction and reactivity in human ALS models
Velásquez, E., Savchenko, E., Marmolejo-Martínez-Artesero, S., Challuau, D., Aebi, A., Pomeshchik, Y., Lamas, N. J., Vihinen, M., Rezeli, M., Schneider, B. L., et al. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106687 · Cited by 7
“Accumulated data suggest that glial cells are critical for disease onset and progression (Yamanaka et al., 2008), but the selective expression of mutant SOD1 in MNs does not induce neurodegeneration in mouse models, indicating active involvement of neighboring cells in ALS pathogenesis (Pramatarova…”
BackgroundImpact of metal oxide nanoparticles against biotic stress in plants
Vaishnavi, P., Prakash, N. K. U., Jayanthi, M., Suganthi, M., & Thenmozhi, M. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-91809-1.00006-8 · Cited by 7
Bakavayev, S., Stavsky, A., Argueti-Ostrovsky, S., Yehezkel, G., Fridmann‐Sirkis, Y., Barak, Z., Gitler, D., Israelson, A., & Engel, S. (2023) · Brain · doi:10.1093/brain/awad222 · Cited by 7
Endo, F. (2024) · Neuroscience Research · doi:10.1016/j.neures.2024.07.008 · Cited by 8
“Conversely, astrocyte-specific reduction of mutant SOD1 slowed disease progression in SOD1 G37R mice (Yamanaka et al., 2008), accompanied by a reduction in TGF-β 1 levels within astrocytes and markers of astrocyte reactivity evidenced by GFAP levels, highlighting a detrimental role of astrocytic…”
BackgroundAnimal Models for Neurodegenerative Disorders
Tsuiji, H., & Yamanaka, K. (2013) · Elsevier eBooks · doi:10.1016/b978-0-12-416002-6.00003-1 · Cited by 7
Self-citationEgawa, N., Suzuki, H., Takahashi, R., Hayakawa, K., Li, W., Lo, E. H., Arai, K., & Inoue, H. (2020) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x20910324 · Cited by 8
“Oligodendrocytes, microglia and astrocytes with mutation of responsive gene SOD1 for familial ALS mutation accelerate disease progression.(10) However, astrocytic NF-kB activation drives microglial proliferation that is rather protective against ALS disease progression in the pre-symptomatic phase.”
BackgroundSelf-citationHashimoto, Y., Yamasaki, R., Ko, S., Matsuo, E., Kobayakawa, Y., Masaki, K., Matsuse, D., & Isobe, N. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232416046 · Cited by 8
“Moreover, loss of mSOD1 in astrocytes delayed the disease progression of ALS [15,16].”
BackgroundUnique nuclear vacuoles in the motor neurons of conditional ADAR2-knockout mice
Sasaki, S., Yamashita, T., Hideyama, T., & Kwak, S. (2014) · Brain Research · doi:10.1016/j.brainres.2014.01.006 · Cited by 7
Yamashita, H., Komine, O., Fujimori-Tonou, N., & Yamanaka, K. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.1045647 · Cited by 7
“Since non-cell autonomous mechanisms have been shown to be involved in the pathology of ALS (Boillée et al., 2006; Yamanaka et al., 2008), it is important to analyze the glial cells surrounding motor neurons such as microglia and astrocytes, in addition to the degenerating motor neurons, to elucidate the pathophysiolo…”
BackgroundMethodSelf-citationA(a)LS: Ammonia-induced amyotrophic lateral sclerosis
Parekh, B. K. (2015) · F1000Research · doi:10.12688/f1000research.6364.1 · Cited by 7
“4 The cellular histological features, explained by ammonia‘s toxicity, includeaxon swelling, blood brain 5 barrier breakdown andastrogliosis and microgliosis[131-133].”
BackgroundActualités dans la recherche fondamentale et clinique sur la sclérose latérale amyotrophique
Pradat, P., Camdessanché, J., Carluer, L., Cintas, P., Corcia, P., Danel-Brunaud, V., Echaniz‐Laguna, A., Gonzalez, J., Nicolas, G., Vandenberghe, N., et al. (2009) · Revue Neurologique · doi:10.1016/j.neurol.2009.01.038 · Cited by 7
Goffin, L., Lemoine, D., & Clotman, F. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1434404 · Cited by 7
Li, D., Wei, Y., Yang, R., Luo, X., Liu, Y., Zhao, W., Yang, H., Wu, Y., Wang, Y., & Huang, Z. (2025) · Theranostics · doi:10.7150/thno.113599 · Cited by 7
Excitotoxicity in amyotrophic lateral sclerosis: a key pathogenic mechanism
Silva-Hucha, S., Hernández, R. G., Baena-López, D., de Sevilla, M. E. F., Paradas, C., & Morcuende, S. (2026) · Brain Communications · doi:10.1093/braincomms/fcag098 · Cited by 7
“84 85-87 One of the first mechanisms proposed to underlie ALS is glutamate excitotoxicity, as stated previously, which is the excessive activation of motor neurons that results from a failure of rapid synaptic glutamate clearance.”
Role of dysregulated calcium homeostasis in astrocytes in neurodegenerative disorders
Sanchez-Mico, M. V., Calvo-Rodríguez, M., & Bacskai, B. J. (2026) · Nature reviews. Neuroscience · doi:10.1038/s41583-026-01032-6 · Cited by 9
“In mutant SOD1 ALS mouse models, selective Cre-mediated excision of mutant SOD1 in astrocytes reduces microglial activation and modestly slows late-stage disease progression, indicating that astrocytic mutant SOD1 contributes to non-cell-autonomous neurotoxicity 232 .”
Respiratory pathology in the TDP-43 transgenic mouse model of amyotrophic lateral sclerosis
Biswas, D. D., Sethi, R., Woldeyohannes, Y., Scarrow, E. R., Haddad, L. E., Lee, J., & ElMallah, M. K. (2024) · Frontiers in Physiology · doi:10.3389/fphys.2024.1430875 · Cited by 6
“(Yamanaka et al., 2008; Frakes et al., 2014; Rojas et al., 2014; Ban et al., 2019; Tam et al., 2019; You et al., 2023).”
Stanaszek, L., Rogujski, P., Drela, K., Fiedorowicz, M., Walczak, P., Łukomska, B., & Janowski, M. (2022) · Antioxidants · doi:10.3390/antiox11061050 · Cited by 6
“Indeed, it was shown that reduction in SOD1 expression in astrocytes results in a delay of disease progression or onset of the disease as well as reduced microglia activation [11].”
BackgroundTargeting low levels of MIF expression as a potential therapeutic strategy for ALS
Alfahel, L., Gschwendtberger, T., Kozareva, V., Dumas, L., Gibbs, R., Kertser, A., Baruch, K., Zaccai, S., Kahn, J., Thau‐Habermann, N., et al. (2024) · Cell Reports Medicine · doi:10.1016/j.xcrm.2024.101546 · Cited by 6
Yamashita, S., Kimura, E., Yamamoto, F., Migita, A., Kanda, E., Mita, S., Teramoto, H., & Uchino, M. (2009) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2009.03.010 · Cited by 6
“Recent research demonstrates thatmutant SOD1within macrophages/microglial cells or astrocytes accelerates disease progression, whereas mutant action within the motor neurons is a primary determinant of onset and early disease [11–13].”
Sclérose latérale amyotrophique, jonction neuromusculaire et déficit énergétique
Dupuis, L., & Loeffler, J. (2008) · médecine/sciences · doi:10.1051/medsci/200824121077 · Cited by 6
“À l’appui de cette hypothèse, la diminution de l’expression de la SOD1 mutée spécifiquement dans les astrocytes retarde la progression des symptômes [21].”
BackgroundMotoneuron Disease: Basic Science
Ilieva, H. S., & Maragakis, N. J. (2017) · Advances in neurobiology · doi:10.1007/978-3-319-57193-5_6 · Cited by 6
Solving the Puzzle of Neurodegeneration
Wolfe, M. S. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811304-2.00001-8 · Cited by 6
Cellular and molecular phenotypes of C9orf72 ALS/FTD patient derived iPSC-microglia mono-culturesPreprint
Lorenzini, I., Alsop, E. B., Levy, J., Gittings, L. M., Lall, D., Rabichow, B. E., Moore, S. R., Pevey, R. S., Bustos, L. M., Burciu, C., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.09.03.277459 · Cited by 6
Sympathetic neuropathology is revealed in muscles affected by amyotrophic lateral sclerosis
Mazzaro, A., Vita, V., Ronfini, M., Casola, I., Klein, A., Dobrowolny, G., Sorarú, G., Musarò, A., Mongillo, M., & Zaglia, T. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1165811 · Cited by 5
“, degeneration and death) is influenced by the expression of mutations in cells which interact, with various biological roles, with MNs, including astrocytes (Clement et al., 2003; Yamanaka et al., 2008; Ziff et al., 2022).”
BackgroundGouveia, D., Correia, J., Cardoso, A., Carvalho, C., Oliveira, A. C., de Almeida, A. P., Gamboa, Ó., Ribeiro, L., Branquinho, M., Sousa, A. C., et al. (2023) · Frontiers in Veterinary Science · doi:10.3389/fvets.2023.1192744 · Cited by 7
Ratano, P., Cocozza, G., Pinchera, C., Busdraghi, L. M., Cantando, I., Martinello, K., Scioli, M., Rosito, M., Bezzi, P., Fucile, S., et al. (2024) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1333745 · Cited by 5
Naito, M., Hideyama, T., Teramoto, S., Saito, T., Kato, H., Terashi, H., Kwak, S., & Aizawa, H. (2022) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2022.120520 · Cited by 5
Urban, M. W., Charsar, B. A., Heinsinger, N. M., Markandaiah, S. S., Sprimont, L., Zhou, W., Brown, E. V., Henderson, N. T., Thomas, S. J., Ghosh, B., et al. (2023) · eLife · doi:10.7554/elife.89298 · Cited by 7
“Given that previous work showed that astrocytes contribute to disease progression in mutant SOD1 rodents post-disease onset ( Yamanaka et al., 2008 ), we examined whether ephrinB2 knockdown in astrocytes extended disease 4.”
BackgroundTomiyama, A. L. M. R., Cartarozzi, L. P., Coser, L. D. O., Chiarotto, G. B., & de Oliveira, A. L. R. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1211486 · Cited by 5
Christou, Y. A., Ohyama, K., Placzek, M., Monk, P. N., & Shaw, P. J. (2013) · BMC Neuroscience · doi:10.1186/1471-2202-14-126 · Cited by 5
“Discussion Published studies over the last few years have demonstrated negative effects of mutant SOD1 astrocytes on MN survival [12-14,17] but no study has so far examined any potential effects on MN progenitor cells.”
BackgroundGamisoyo-San Ameliorates Neuroinflammation in the Spinal Cord of hSOD1G93A Transgenic Mice
Cai, M., & Yang, E. J. (2018) · Mediators of Inflammation · doi:10.1155/2018/5897817 · Cited by 5
“mSOD1 deletion in astrocytes and microglia of hSOD1 mice has been shown to prolong survival [13, 35].”
BackgroundSilva, T. M., Borniger, J. C., Alves, M. J., Alzate‐Correa, D., Zhao, J., Fadda, P., Toland, A. E., Takakura, A. C. T., Moreira, T. S., Czeisler, C. M., et al. (2021) · Journal of Neurophysiology · doi:10.1152/jn.00155.2020 · Cited by 4
Neuroinflammation in amyotrophic lateral sclerosis
Endo, F., & Yamanaka, K. (2014) · Rinsho Shinkeigaku · doi:10.5692/clinicalneurol.54.1128 · Cited by 5
Self-citationAmyotrophic Lateral Sclerosis and Other Motor Neuron Diseases
Shaw, P. J. (2012) · Elsevier eBooks · doi:10.1016/b978-1-4377-1604-7.00418-8 · Cited by 5
Amyotrophic lateral sclerosis: mechanisms and therapeutic strategies
Bosch, L. V. D. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-805120-7.00011-7 · Cited by 5
Schmitt, N. D., Rawlins, C. M., Randall, E. C., Wang, X., Koller, A. A., Auclair, J. R., Kowalski, J., Kowalski, P. J., Luther, E., Ivanov, A. R., et al. (2019) · Analytical Chemistry · doi:10.1021/acs.analchem.8b03454 · Cited by 5
Neuroglia in Neurological Diseases
Verkhratsky, A., & Butt, A. M. (2013) · Wiley eBooks · doi:10.1002/9781118402061.ch10 · Cited by 5
Mei, I., Nichterwitz, S., Lebœuf, M., Nijssen, J., Lenoël, I., Repsilber, D., Lobsiger, C. S., & Hedlund, E. (2025) · Genome Research · doi:10.1101/gr.279501.124 · Cited by 5
Columbro, S. F., Tortarolo, M., Cecconi, A. D. R., Piccirillo, R., Bendotti, C., Biasini, E., Pasetto, L., & Bonetto, V. (2025) · Experimental Neurology · doi:10.1016/j.expneurol.2025.115521 · Cited by 4
Curing the brain: in search for new astrocyte-specific therapies
Verkhratsky, A., Lee, C. J., Chun, H., Göritz, C., Harkany, T., Lee, J., Lee, S., Lindskog, M., Koh, W., Mulder, J., et al. (2026) · Experimental & Molecular Medicine · doi:10.1038/s12276-026-01712-4 · Cited by 8
“…dismutase 1 (SOD1 G93A ) mutant gene to replicate ALS in mice further highlighted the primary role of astrocyte: astrocyte-selective silencing of SOD1 alleviated ALS symptoms and increased life span 240,241 , whereas restricted expression of SOD1 in neurons did not cause pathology 242,243 .”
Misawa, H., Kamishima, K., Koyama, T., Ohgaki, L., Morisaki, Y., Yamanaka, T., Itohara, S., Sawano, S., Mizunoya, W., & Ogihara, N. (2024) · Experimental Neurology · doi:10.1016/j.expneurol.2024.114772 · Cited by 4
Self-citationTournezy, J., Léger, C., Klonjkowski, B., Gonzalez‐Dunia, D., Szelechowski, M., Garenne, A., Mathis, S., Chevallier, S., & Masson, G. L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252312789 · Cited by 4
“The removal of mSOD1 in either microglia or astrocytes extends the survival of mice by slowing disease progression but does not delay the onset of the disease [20,37].”
Vaccine Based Approaches for the Prevention and Treatment of Neurological Disease
Aderinto, N., Abraham, I. C., Olatunji, G. D., Kokori, E., Ashinze, P. T., Babawale, E. A., Alabi, B. O., Opeyemi, O. D., Babalola, A. E., Ayoola, O. I., et al. (2025) · Current Treatment Options in Neurology · doi:10.1007/s11940-025-00827-9 · Cited by 5
“Additionally, vaccines targeting specific TDP-43 epitopes have demonstrated potential in preclinical models, stimulating antibody production that selectively reacts to the misfolded protein while minimizing autoimmune responses [95].”
Perera, N. D., Silva, S. D., Tomas, D., Cuic, B., & Turner, B. J. (2025) · Glia · doi:10.1002/glia.70045 · Cited by 3
“Findings from the last decade suggest ALS progression might be attributed to non-cell autonomous mechanisms from glia (Boillée et al. 2006; Yamanaka et al. 2008).”
The Neuroinflammation in the Physiopathology of Amyotrophic Lateral Sclerosis
Bowerman, M., Vincent, T., Scamps, F., Camu, W., & Raoul, C. (2013) · InTech eBooks · doi:10.5772/56489 · Cited by 5
“Given the relationship between astrocytes and microglia [17, 84] and the importance of astrocytosis in ALS, it has been hypothesized that microgliosis may also participate in ALS pathogenesis.”
BackgroundWhy is ALS so Difficult to Treat?
Turnbull, J. (2014) · Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques · doi:10.1017/s0317167100016516 · Cited by 4
A Glutamate Scavenging Protocol Combined with Deanna Protocol in SOD1-G93A Mouse Model of ALS
Rogers, C. Q., Ramirez, M., Landon, C. S., DeBlasi, J. M., Koutnik, A. P., Ari, C., & D’Agostino, D. P. (2023) · Nutrients · doi:10.3390/nu15081821 · Cited by 4
Gil, R. S., Clarke, B. E., Ecroyd, H. W., Kalmár, B., & Greensmith, L. (2021) · Cells · doi:10.3390/cells10051257 · Cited by 4
Multiple Routes of Motor Neuron Degeneration in ALS
Hee, J., & Keun, J. S. (2013) · InTech eBooks · doi:10.5772/56625 · Cited by 5
Excitotoxicity and Amyotrophic Lateral Sclerosis
Staats, K. A., & Bosch, L. V. D. (2022) · Springer eBooks · doi:10.1007/978-3-031-15080-7_147 · Cited by 4
Nava, J. L. G. (2014) · doi:10.26481/dis.20141209jg · Cited by 4
Burg, T., Bichara, C., Scekic‐Zahirovic, J., Fischer, M., Stuart‐Lopez, G., Lefèbvre, F., Cordero‐Erausquin, M., & Rouaux, C. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/849935 · Cited by 4
“Such approaches have allowed to better define the contributions of MN [4], microglia [4,68], astrocytes [69] and muscles [45] to ALS onset and progression.”
BackgroundAlhathli, E. M., Cooper‐Knock, J., Girach, Z.-U.-A., Julian, T. H., Bauer, C. S., Timmons, H. O., Ward, B. D., Walker, H., Azzouz, M., Elrayess, M. A., et al. (2026) · BMC Medicine · doi:10.1186/s12916-026-04727-w · Cited by 3
Interplay between codon usage and ribosome heterogeneity: A new layer of translational regulation
Dahal, U., Bansal, A., Dahal, A. R., Aryal, M. R., & Khanal, B. (2025) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2025.152971 · Cited by 3
Metadata
- Authors
- Yamanaka, K., Chun, S. J., Boillee, S., Fujimori-Tonou, N., Yamashita, H., Gutmann, D. H., Takahashi, R., Misawa, H., & Cleveland, D. W.
- Affiliations
- University of California San Diego (US)
- RIKEN Center for Brain Science (JP)
- Corresponding author
- Yamanaka, Koji
- Cleveland, Don W
- Venue
- Nature Neuroscience
- Published
- 2008-02-03
- Volume
- 11
- Issue
- 3
- Pages
- 251-253
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3137510
- OpenAlex
- W2068147651
- Cited by
- 1,140
- References
- 15
- Citations by year
- 2026: 29 · 2025: 30 · 2024: 40 · 2023: 68 · 2022: 50 · 2021: 46 · 2020: 60 · 2019: 63 · 2018: 66 · 2017: 71 · 2016: 64 · 2015: 77 · 2014: 86 · 2013: 72 · 2012: 77
- FWCI
- 51.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS 27036, R37NS027036, R01NS027036)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Keywords
- astrocytes, amyotrophic lateral sclerosis, superoxide dismutase 1, SOD1 mutations, non-cell autonomous neurodegeneration, motor neuron degeneration, microglial activation, disease progression, astrocyte-targeted therapy, mouse model
- MeSH terms
- Superoxide Dismutase-1, Amyotrophic Lateral Sclerosis, Animals, Astrocytes, Disease Models, Animal, Genes, Dominant, Glial Fibrillary Acidic Protein, Gliosis, Humans, Mice, Transgenic, Mutation, Nerve Degeneration, Nitric Oxide, Spinal Cord, Superoxide Dismutase, Genetic Therapy, Survival Rate, Cell Death, Microglia, Oxidative Stress, Disease Progression, Integrases, Mice, Nitric Oxide Synthase Type II
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
