The DOI matches its Crossref record; 114 of the 114 references it cites were found in a registry or an index.
Clinical Spectrum of Amyotrophic Lateral Sclerosis (ALS)
Open accessAbstract
Amyotrophic lateral sclerosis (ALS) is primarily characterized by progressive loss of motor neurons, although there is marked phenotypic heterogeneity between cases. Typical, or "classical," ALS is associated with simultaneous upper motor neuron (UMN) and lower motor neuron (LMN) involvement at disease onset, whereas atypical forms, such as primary lateral sclerosis and progressive muscular atrophy, have early and predominant involvement in the UMN and LMN, respectively. The varying phenotypes can be so distinctive that they would seem to have differing biology. Because the same phenotypes can have multiple causes, including different gene mutations, there may be multiple molecular mechanisms causing ALS, implying that the disease is a syndrome. Conversely, multiple phenotypes can be caused by a single gene mutation; thus, a single molecular mechanism could be compatible with clinical heterogeneity. The pathogenic mechanism(s) in ALS remain unknown, but active propagation of the pathology neuroanatomically is likely a primary component.
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Cites
Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis
Neumann, M., Sampathu, D. M., Kwong, L. K., Truax, A. C., Micsenyi, M. C., Chou, T. T., Bruce, J., Schuck, T., Grossman, M., Clark, C. M., et al. (2006) · Science · doi:10.1126/science.1134108 · Cited by 6,576
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“Additionally, the single most common genetic cause of either ALS or FTD is mutation in C9ORF72, which can cause either disease or an overlap of the two (DeJesus-Hernandez et al. 2011; Renton et al. 2011).”
BackgroundA Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD
Renton, A. E., Majounie, E., Waite, A., Simón-Sánchez, J., Rollinson, S., Gibbs, J. R., Schymick, J. C., Laaksovirta, H., van Swieten, J. C., Myllykangas, L., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.010 · Cited by 4,409
Arai, T., Hasegawa, M., Akiyama, H., Ikeda, K., Nonaka, T., Mori, H., Mann, D., Tsuchiya, K., Yoshida, M., Hashizume, Y., et al. (2006) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2006.10.093 · Cited by 2,732
Neurodegenerative Diseases Target Large-Scale Human Brain Networks
Seeley, W. W., Crawford, R. K., Zhou, J., Miller, B. L., & Greicius, M. D. (2009) · Neuron · doi:10.1016/j.neuron.2009.03.024 · Cited by 2,350
State of play in amyotrophic lateral sclerosis genetics
Renton, A. E., Chiò, A., & Traynor, B. J. (2014) · Nature Neuroscience · doi:10.1038/nn.3584 · Cited by 1,544
ALS: A Disease of Motor Neurons and Their Nonneuronal Neighbors
Boillée, S., Vande Velde, C., & Cleveland, D. W. (2006) · Neuron · doi:10.1016/j.neuron.2006.09.018 · Cited by 1,429
From charcot to lou gehrig: deciphering selective motor neuron death in als
Cleveland, D. W., & Rothstein, J. D. (2001) · Nature Reviews Neuroscience · doi:10.1038/35097565 · Cited by 1,389
Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS
Elden, A. C., Kim, H.-J., Hart, M. P., Chen-Plotkin, A. S., Johnson, B. S., Fang, X., Armakola, M., Geser, F., Greene, R., Lu, M. M., et al. (2010) · Nature · doi:10.1038/nature09320 · Cited by 1,325
The C9orf72 GGGGCC Repeat Is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS
Mori, K., Weng, S.-M., Arzberger, T., May, S., Rentzsch, K., Kremmer, E., Schmid, B., Kretzschmar, H. A., Cruts, M., Van Broeckhoven, C., et al. (2013) · Science · doi:10.1126/science.1232927 · Cited by 1,277
Cited by
Role of Edaravone as a Treatment Option for Patients with Amyotrophic Lateral Sclerosis
Cho, H., & Shukla, S. (2020) · Pharmaceuticals · doi:10.3390/ph14010029 · Cited by 124
Pun, F. W., Liu, B. H. M., Long, X., Leung, H. W., Leung, G. H. D., Mewborne, Q. T., Gao, J., Shneyderman, A., Ozerov, I. V., Wang, J., et al. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.914017 · Cited by 115
“ALS can be categorized based on its root causes - familial or sporadic (Grad et al., 2017).”
BackgroundCellular Compartmentalization, Glutathione Transport and Its Relevance in Some Pathologies
Vázquez-Meza, H., Vilchis-Landeros, M. M., Vázquez-Carrada, M., Uribe-Ramírez, D., & Matuz-Mares, D. (2023) · Antioxidants · doi:10.3390/antiox12040834 · Cited by 94
Genetically modified large animal models for investigating neurodegenerative diseases
Yang, W., Chen, X., Li, S., & Li, X.-J. (2021) · Cell & Bioscience · doi:10.1186/s13578-021-00729-8 · Cited by 45
Morini, E., Portaro, S., Leonetti, D., De Cola, M. C., De Luca, R., Bonanno, M., Quartarone, A., & Calabrò, R. S. (2023) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph20042923 · Cited by 11
Metadata
- Authors
- Grad, L. I., Rouleau, G. A., Ravits, J., & Cashman, N. R.
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2016-12-21
- Volume
- 7
- Issue
- 8
- Pages
- a024117
- ISSN
- 2157-1422 (ISSN-L)
- OpenAlex
- W2564558365
- Cited by
- 316
- References
- 114
- Type
- posted content
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Clinical Spectrum of Amyotrophic Lateral Sclerosis (ALS). https://app.cochat.ai/papers/10.1101/cshperspect.a024117
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- Grad, L. I., Rouleau, G. A., Ravits, J., & Cashman, N. R. (2017). Clinical Spectrum of Amyotrophic Lateral Sclerosis (ALS). Cold Spring Harbor Perspectives in Medicine. https://doi.org/10.1101/cshperspect.a024117
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
