Neurodegenerative diseases: a decade of discoveries paves the way for therapeutic breakthroughs
By M. Forman, John Q. Trojanowski, V. Lee. Nature Medicine, 2004
724 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/b893d607200fb51c62d045d6bae401b381ed94c9
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
- V. Lee
- John Q. Trojanowski
- H. Ko
- T. Kam
- Nikhil Panicker
- D. Sinclair
- Li-Huei Tsai
- Daniel H. Geschwind
In Molecular Biology
- Oliver D. King
- Li-Huei Tsai
- John Q. Trojanowski
- Michael Jeffrey Gandal
- Neelroop Parikshak
- J. Shorter
- Aaron Gitler
- D. Sinclair
In Physiology
- V. Lee
- John Q. Trojanowski
- D. Sinclair
- Joseph A. Baur
- P. Shaw
- Li-Huei Tsai
- Nigel J. Cairns
- Daniel H. Geschwind
Citations in the corpus
- Systems biology and gene networks in neurodevelopmental and neurodegenerative disorders (2015, background): “…of these diseases have known causes that involve mutations in ubiquitously expressed proteins 134 , but they follow stereotyped patterns of degeneration that selectively affect certain cell subsets more severely, resulting in disease-specific spatial and temporal patterns of degeneration 135–137 .”
- Pathological TDP‐43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations (2007, background): “This sort of accumulation of insoluble, misfolded proteins in neurons is a common feature of many neurodegenerative disorders and has been speculated to cause cellular dysfunction by interfering with essential processes such as intracellular transport.(28) Furthermore, cells that contain TDP-43–posi”
- Transneuronal Propagation of Pathologic α-Synuclein from the Gut to the Brain Models Parkinson's Disease. (2019, background): “It is likely that separate and combinatory processes of initiation via nasal and/or gastric routes and spread contribute to PD and DLB, and in some patients, there may be a dual hit (Hawkes et al., 2007).”
- Stress granules as crucibles of ALS pathogenesis (2013, background): “Like several other neurodegenerative diseases, the degenerating neurons of ALS patients are characterized by the accumulation of protein aggregates (Forman et al., 2004).”
- Identification of pre-clinical Alzheimer’s disease by a profile of pathogenic proteins in neurally-derived blood exosomes: a case-control study (2014, background): “008 side and on the surface of neurons [1,2].”
- Traumatic brain injury: a disease process, not an event. (2010, background): “Ab plaques and neurofibrillary tangles comprised of tau protein are pathological characteristics of AD (Braak and Braak, 1991; Forman et al., 2004).”
- Tau-mediated neurodegeneration in Alzheimer's disease and related disorders (2007, background): “Tau-mediated neurodegeneration As described above, in AD and related neurodegenerative disorders that are collectively referred to as tauopathies”
- SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis (2007, background): “…neurodegenera- tion raises the possibility of developing a class of therapeutic interventions that treat a variety of neurological disorders by activating the body’s own defenses against age-related dete- rioration and cell death (Bossy-Wetzel et al, 2004; Forman et al, 2004; Selkoe, 2004).”