Amyotrophic lateral sclerosis.

By A. Ludolph, J. Brettschneider, Jochen H Weishaupt. Current Opinion in Neurology, 2012

6,780 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Genetics, Neurology

View Paper: https://www.semanticscholar.org/paper/593e5c0f33c6eb6a2c3600c4e1ffc79525fefe37

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Eric W. Sellers
2. Jonathan R. Wolpaw
3. Theresa M. Vaughan
4. L. Zuo
5. Chunyan Guo
6. A. Strasser
7. Zewen Liu
8. Xueping Chen

In Genetics

1. Robert H. Brown
2. Can Alkan
3. Evan E. Eichler
4. Jeffrey D. Rothstein
5. David E. Heckerman
6. Clifford J. Woolf
7. I. Slaninová
8. Computational Pan-Genomics Consortium

In Neurology

1. Henrik Zetterberg
2. Kaj Blennow
3. Robert H. Brown
4. Pegah Masrori
5. D. Bailey
6. P. van Damme
7. L. Zuo
8. Zewen Liu

Citations in the corpus

• Intrinsic Membrane Hyperexcitability of ALS Patient-Derived Motor Neurons (2014, background): “Amyotrophic lateral sclerosis (ALS) is a devastating, untreatable disease of upper and lower motor neurons (Kiernan et al., 2011).”
• Evaluating drug targets through human loss-of-function genetic variation (2019, neutral): “One a meta-analysis found that ~4.6% of ALS is familial 71 , although a figure of 10% is also often used 72 .”
• A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD (2011, background): “Amyotrophic lateral sclerosis (ALS, OMIM #105400) is a fatal neurodegenerative disease characterized clinically by progressive paralysis leading to death from respiratory failure, typically within two to three years of symptom onset (Rowland and Shneider, 2001).”
• A brain-computer interface for long-term independent home use (2010, background): “With home ventilators and other support equipment, people with ALS can lead long and ful­ filling lives despite their extreme disability (4).”
• Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. (2010, background): “connecting the spinal cord and brain stem to muscle fibers, leading to muscle denervation and atrophy [1].”
• Oxidative Stress in Neurodegenerative Diseases: From Molecular Mechanisms to Clinical Applications (2017, background): “Amyotrophic lateral sclerosis (ALS) is characterized by progressive loss of motor neurons in the anterior horn of the spinal cord [111, 112].”
• Amyotrophic lateral sclerosis: a clinical review (2020, background): “Multiple molecular pathways have been implicated in the pathogenesis of ALS, such as failure of proteostasis, excitotoxicity, neuroinflammation, mitochondrial dysfunction and oxidative stress, oligodendrocyte dysfunction, cytoskeletal disturbances and axonal transport defects, disturbed RNA metaboli”
• Oxidative stress in neurodegenerative diseases (2012, background): “Amyotrophic lateral sclerosis is characterized by the degeneration of, primarily, spinal motor neurons, but also cortical and brain stem neurons [27] .”
• Exome sequencing reveals VCP mutations as a cause of familial ALS (2010, positive): “The identification of genes underlying rare familial forms of ALS has had significant impact on our understanding of the molecular mechanisms underlying typical ALS (Rowland and Shneider, 2001).”
• Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, neutral): “Glutamate-mediated excitotoxicity is another possible mechanism that is proposed in the pathogenesis of ALS (Reviewed in Rowland and Shneider, 2001).”
• Neuronal calcium signaling: function and dysfunction (2014, background): “The perturbation of cellular Ca2+ homeostasis is now increasingly considered to be important in the pathogenesis of ALS [132, 133]: it may involve malfunctions of membrane channels and/or of the mitochondrial Ca2+ controlling systems, as well as alterations in the Ca2+-buffering capacity of proteins”